AbstractProstate cancer is one of the most commonly diagnosed cancers in men and is a major cause of cancer-related deaths worldwide. Among the molecular processes that contribute to this disease, the weight of metabolism has been placed under the limelight in recent years. Tumours exhibit metabolic adaptations to comply with their biosynthetic needs.

摘要前列腺癌是男性最常见的癌症之一，是全球癌症相关死亡的主要原因。在导致这种疾病的分子过程中，代谢的重要性近年来一直备受关注。。

However, metabolites also play an important role in supporting cell survival in challenging environments or remodelling the tumour microenvironment, thus being recognized as a hallmark in cancer. Prostate cancer is uniquely driven by androgen receptor signalling, and this knowledge has also influenced the paths of cancer metabolism research.

然而，代谢物在支持具有挑战性的环境中的细胞存活或重塑肿瘤微环境方面也起着重要作用，因此被认为是癌症的标志。前列腺癌是由雄激素受体信号传导独特驱动的，这一知识也影响了癌症代谢研究的途径。

This review provides a comprehensive perspective on the metabolic adaptations that support prostate cancer progression beyond androgen signalling, with a particular focus on tumour cell intrinsic and extrinsic pathways..

这篇综述提供了一个关于支持前列腺癌进展超出雄激素信号传导的代谢适应的全面观点，特别关注肿瘤细胞内在和外在途径。。

IntroductionThe androgen receptor (AR) is a central player in the biology of the prostate, operating as a nuclear receptor essential for normal prostate development and function [1]. AR mediates the effects of androgens and regulates the expression of genes involved in prostate growth, maintenance, and differentiation.

。AR介导雄激素的作用并调节参与前列腺生长，维持和分化的基因的表达。

Beyond developmental stages, AR also influences prostate health throughout adulthood [2]. AR signalling is linked to the onset and progression of prostate cancer (PCa), where it becomes a primary driver of tumour growth. Therefore, inhibition of AR function represents the targeted therapy in this disease [3].

除了发育阶段，AR还影响整个成年期的前列腺健康（2）。AR信号传导与前列腺癌（PCa）的发生和发展有关，它成为肿瘤生长的主要驱动因素。因此，抑制AR功能代表了该疾病的靶向治疗（3）。

AR reprograms PCa cellular metabolism, creating a unique molecular scenario that has been documented for the last 100 years [4]. Nevertheless, the complexity underlying cellular metabolism extends beyond AR signalling, which is envisioned to offer innovative therapeutic opportunities. Our current understanding of cellular metabolism encompasses aspects such as the tumour microenvironment (TME) or diet.

AR重新编程PCa细胞代谢，创造了一个独特的分子场景，已经记录了过去100年（4）。然而，细胞代谢的复杂性超出了AR信号传导的范围，这有望提供创新的治疗机会。我们目前对细胞代谢的理解包括肿瘤微环境（TME）或饮食等方面。

In this review, we will explore major metabolic pathways supporting PCa progression and metastasis, with special emphasis on tumour cell-intrinsic and extrinsic glucose, lipid and one-carbon metabolism (1 C metabolism), while other relevant processes including the connection between metabolism and epigenetics will be left out of the scope of this work.

在这篇综述中，我们将探索支持PCa进展和转移的主要代谢途径，特别强调肿瘤细胞内在和外在的葡萄糖，脂质和单碳代谢（1C代谢），而其他相关过程，包括代谢和表观遗传学之间的联系将被排除在这项工作的范围之外。

Furthermore, we will incorporate new evidence from other tumour types to identify shared characteristics that can apply to PCa.Major metabolic alterations in prostate cancer cellsGlucose metabolismGlycolysis and the Warburg effectGlycolysis metabolises glucose to pyruvate via a series of intermediate reactions, generating ATP and NADH (Fig. 1).

此外，我们将纳入其他肿瘤类型的新证据，以确定可应用于PCa的共同特征。前列腺癌细胞的主要代谢改变葡萄糖代谢糖酵解和Warburg效应糖酵解通过一系列中间反应将葡萄糖代谢为丙酮酸，产生ATP和NADH（图1）。

Cancer cells often exhibit increased glycolytic activity to .

癌细胞通常表现出增加的糖酵解活性。

ReferencesHeinlein CA, Chang C. Androgen receptor in prostate cancer. Endocr Rev. 2004;25:276–308.CAS

参考文献Heinlein CA，Chang C.前列腺癌中的雄激素受体。Endocr Rev.2004；25:276–308.CAS

PubMed

PubMed

Google Scholar

谷歌学者

Gibson DA, Saunders PTK, McEwan IJ. Androgens and androgen receptor: above and beyond. Mol Cell Endocrinol. 2018;465:1–3.CAS

吉布森DA，桑德斯PTK，麦克尤恩IJ。雄激素和雄激素受体：超越。摩尔细胞内分泌。2018年；465:1-3.CAS

PubMed

PubMed

Google Scholar

谷歌学者

Dehm SM, Tindall DJ. Molecular regulation of androgen action in prostate cancer. J Cell Biochem. 2006;99:333–44.CAS

Dehm SM，Tindall DJ。前列腺癌中雄激素作用的分子调控。J细胞生物化学。；99:333–44.CAS

PubMed

PubMed

Google Scholar

谷歌学者

Barfeld SJ, Itkonen HM, Urbanucci A, Mills IG. Androgen-regulated metabolism and biosynthesis in prostate cancer. Endocr Relat Cancer. 2014;21:T57–66.PubMed

Barfeld SJ，Itkonen HM，Urbanucci A，Mills IG。雄激素调节前列腺癌的代谢和生物合成。内分泌相关癌症。2014年；21:T57–66.PubMed

Google Scholar

谷歌学者

Warburg O, Wind F, Negelein E. The metabolism of tumors in the body. J Gen Physiol. 1927;8:519–30.CAS

Warburg O，Wind F，Negelein E.体内肿瘤的代谢。J Gen生理学。1927年；8： 519–30.CAS

PubMed

PubMed

PubMed Central

公共医学中心

Google Scholar

谷歌学者

DeBerardinis RJ, Chandel NS. We need to talk about the Warburg effect. Nat Metab. 2020;2:127–9.PubMed

DeBerardinis RJ，Chandel NS。我们需要谈谈沃伯格效应。自然代谢。2020年；2： 127-9.PubMed

Google Scholar

谷歌学者

Luengo A, Li Z, Gui DY, Sullivan LB, Zagorulya M, Do BT, et al. Increased demand for NAD(+) relative to ATP drives aerobic glycolysis. Mol Cell. 2021;81:691–707.e6.CAS

Luengo A，Li Z，Gui DY，Sullivan LB，Zagorulya M，Do BT等。相对于ATP，对NAD（+）的需求增加会驱动有氧糖酵解。摩尔细胞。2021年；81:691–707.e6.CAS

PubMed

PubMed

Google Scholar

谷歌学者

Wang Y, Stancliffe E, Fowle-Grider R, Wang R, Wang C, Schwaiger-Haber M, et al. Saturation of the mitochondrial NADH shuttles drives aerobic glycolysis in proliferating cells. Mol Cell. 2022;82:3270–83.e9.CAS

Wang Y，Stancliffe E，Fowle Grider R，Wang R，Wang C，Schwaiger-Haber M等。线粒体NADH穿梭的饱和驱动增殖细胞中的有氧糖酵解。摩尔细胞。2022年；82:3270–83.e9.CAS

PubMed

PubMed

PubMed Central

公共医学中心

Google Scholar

谷歌学者

Vaarwerk B, Breunis WB, Haveman LM, de Keizer B, Jehanno N, Borgwardt L, et al. Fluorine-18-fluorodeoxyglucose (FDG) positron emission tomography (PET) computed tomography (CT) for the detection of bone, lung, and lymph node metastases in rhabdomyosarcoma. Cochrane Database Syst Rev.

Vaarwerk B，Breunis WB，Haveman LM，de Keizer B，Jehanno N，Borgwardt L等。氟-18-氟脱氧葡萄糖（FDG）正电子发射断层扫描（PET）计算机断层扫描（CT）用于检测横纹肌肉瘤中的骨，肺和淋巴结转移。Cochrane数据库系统修订版。

2021;11:CD012325.PubMed .

2021;11:CD012325。

Google Scholar

谷歌学者

Graham NA, Minasyan A, Lomova A, Cass A, Balanis NG, Friedman M, et al. Recurrent patterns of DNA copy number alterations in tumors reflect metabolic selection pressures. Mol Syst Biol. 2017;13:914.PubMed

Graham NA，Minasyan A，Lomova A，Cass A，Balanis NG，Friedman M等。肿瘤中DNA拷贝数改变的复发模式反映了代谢选择压力。摩尔系统生物学。2017年；13： 914.PubMed

PubMed Central

公共医学中心

Google Scholar

谷歌学者

Wei J, Huang K, Chen Z, Hu M, Bai Y, Lin S, et al. Characterization of glycolysis-associated molecules in the tumor microenvironment revealed by pan-cancer tissues and lung cancer single cell data. Cancers (Basel). 2020;12:1788.CAS

Wei J，Huang K，Chen Z，Hu M，Bai Y，Lin S，等。泛癌组织和肺癌单细胞数据揭示的肿瘤微环境中糖酵解相关分子的表征。癌症（巴塞尔）。2020年；12： 1788年

PubMed

PubMed

Google Scholar

谷歌学者

Mitchell KG, Amini B, Wang Y, Carter BW, Godoy MCB, Parra ER, et al. 18)F-fluorodeoxyglucose positron emission tomography correlates with tumor immunometabolic phenotypes in resected lung cancer. Cancer Immunol Immunother. 2020;69:1519–34.Mathews EH, Liebenberg L, Pelzer R. High-glycolytic cancers and their interplay with the body’s glucose demand and supply cycle.

Mitchell KG，Amini B，Wang Y，Carter BW，Godoy MCB，Parra ER等18）F-氟脱氧葡萄糖正电子发射断层扫描与切除肺癌的肿瘤免疫代谢表型相关。癌症免疫治疗。2020年；69:1519–34.Mathews EH，Liebenberg L，Pelzer R.高糖酵解癌症及其与身体葡萄糖需求和供应周期的相互作用。

Med Hypotheses. 2011;76:157–65.CAS .

医学假说。2011年；76:157-65。CAS。

PubMed

PubMed

Google Scholar

谷歌学者

Uo T, Sprenger CC, Plymate SR. Androgen receptor signaling and metabolic and cellular plasticity during progression to castration resistant prostate cancer. Front Oncol. 2020;10:580617.PubMed

Uo T，Sprenger CC，Plymate SR.雄激素受体信号传导以及去势抵抗性前列腺癌进展过程中的代谢和细胞可塑性。前部Oncol。2020年；10： 580617.PubMed

PubMed Central

公共医学中心

Google Scholar

谷歌学者

White MA, Tsouko E, Lin C, Rajapakshe K, Spencer JM, Wilkenfeld SR, et al. GLUT12 promotes prostate cancer cell growth and is regulated by androgens and CaMKK2 signaling. Endocr Relat Cancer. 2018;25:453–69.CAS

White MA，Tsouko E，Lin C，Rajapakshe K，Spencer JM，Wilkenfeld SR等。GLUT12促进前列腺癌细胞生长，并受雄激素和CaMKK2信号调节。内分泌相关癌症。2018年；25:453–69.CAS

PubMed

PubMed

PubMed Central

公共医学中心

Google Scholar

谷歌学者

Xu M, Sakamoto S, Matsushima J, Kimura T, Ueda T, Mizokami A, et al. Up-regulation of LAT1 during antiandrogen therapy contributes to progression in prostate cancer cells. J Urol. 2016;195:1588–97.PubMed

Xu M，Sakamoto S，Matsushima J，Kimura T，Ueda T，Mizokami A等。抗雄激素治疗期间LAT1的上调有助于前列腺癌细胞的进展。J乌拉尔。；195:1588–97.PubMed

Google Scholar

谷歌学者

Wang J, Xu W, Wang B, Lin G, Wei Y, Abudurexiti M, et al. GLUT1 is an AR target contributing to tumor growth and glycolysis in castration-resistant and enzalutamide-resistant prostate cancers. Cancer Lett. 2020;485:45–55.CAS

Wang J，Xu W，Wang B，Lin G，Wei Y，Abudurexiti M等。GLUT1是一种AR靶标，有助于去势抵抗性和恩扎鲁胺抵抗性前列腺癌的肿瘤生长和糖酵解。癌症Lett。2020年；485:45–55.CAS

PubMed

PubMed

Google Scholar

谷歌学者

de Wet L, Williams A, Gillard M, Kregel S, Lamperis S, Gutgesell LC, et al. SOX2 mediates metabolic reprogramming of prostate cancer cells. Oncogene. 2022;41:1190–202.PubMed

de Wet L，Williams A，Gillard M，Kregel S，Lamperis S，Gutgesell LC等。SOX2介导前列腺癌细胞的代谢重编程。致癌基因。2022年；41:1190–202.PubMed

PubMed Central

公共医学中心

Google Scholar

谷歌学者

Crowell PD, Giafaglione JM, Jones AE, Nunley NM, Hashimoto T, Delcourt AML, et al. MYC is a regulator of androgen receptor inhibition-induced metabolic requirements in prostate cancer. Cell Rep. 2023;42:113221.CAS

Crowell PD，Giafaglione JM，Jones AE，Nunley NM，Hashimoto T，Delcourt AML等。MYC是前列腺癌中雄激素受体抑制诱导的代谢需求的调节剂。细胞代表2023；42:113221.CAS

PubMed

PubMed

Google Scholar

谷歌学者

Liu Y, Zuckier LS, Ghesani NV. Dominant uptake of fatty acid over glucose by prostate cells: a potential new diagnostic and therapeutic approach. Anticancer Res. 2010;30:369–74.PubMed

刘Y，Zuckier LS，Ghesani NV。前列腺细胞对葡萄糖的主要摄取脂肪酸：一种潜在的新诊断和治疗方法。抗癌研究2010；

Google Scholar

谷歌学者

Sadeghi RN, Karami-Tehrani F, Salami S. Targeting prostate cancer cell metabolism: impact of hexokinase and CPT-1 enzymes. Tumour Biol. 2015;36:2893–905.CAS

Sadeghi RN，Karami Tehrani F，Salami S.靶向前列腺癌细胞代谢：己糖激酶和CPT-1酶的影响。肿瘤生物学。2015年；36:2893–905.CAS

PubMed

PubMed

Google Scholar

谷歌学者

Twum-Ampofo J, Fu D-X, Passaniti A, Hussain A, Siddiqui MM. Metabolic targets for potential prostate cancer therapeutics. Curr Opin Oncol. 2016;28:241–7.CAS

Twum Ampofo J，Fu D-X，Passaniti A，Hussain A，Siddiqui MM。潜在前列腺癌治疗的代谢靶点。Curr Opin Oncol公司。；28:241–7.CAS

PubMed

PubMed

PubMed Central

公共医学中心

Google Scholar

谷歌学者

Jadvar H. PET of glucose metabolism and cellular proliferation in prostate cancer. J Nucl Med. 2016;57:25S–9S.CAS

Jadvar H.前列腺癌中葡萄糖代谢和细胞增殖的PET。J Nucl Med。2016；。中科院

PubMed

PubMed

PubMed Central

公共医学中心

Google Scholar

谷歌学者

Vaz CV, Alves MG, Marques R, Moreira PI, Oliveira PF, Maia CJ, et al. Androgen-responsive and nonresponsive prostate cancer cells present a distinct glycolytic metabolism profile. Int J Biochem Cell Biol. 2012;44:2077–84.CAS

Vaz CV，Alves MG，Marques R，Moreira PI，Oliveira PF，Maia CJ等。雄激素反应性和无反应性前列腺癌细胞呈现出独特的糖酵解代谢特征。Int J生物化学细胞生物学。2012年；44:2077-84.CAS

PubMed

PubMed

Google Scholar

谷歌学者

Granlund KL, Tee S-S, Vargas HA, Lyashchenko SK, Reznik E, Fine S, et al. Hyperpolarized MRI of human prostate cancer reveals increased lactate with tumor grade driven by monocarboxylate transporter 1. Cell Metab. 2020;31:105–14.e3.CAS

Granlund KL，Tee S-S，Vargas HA，Lyashchenko SK，Reznik E，Fine S等。人类前列腺癌的超极化MRI显示乳酸增加，肿瘤分级由单羧酸转运蛋白1驱动。细胞代谢。2020年；31:105–14.e3.CAS

PubMed

PubMed

Google Scholar

谷歌学者

Chen M-L, Xu P-Z, Peng X, Chen WS, Guzman G, Yang X, et al. The deficiency of Akt1 is sufficient to suppress tumor development in Pten + /− mice. Genes Dev. 2006;20:1569–74.CAS

Chen M-L，Xu P-Z，Peng X，Chen WS，Guzman G，Yang X等。Akt1的缺乏足以抑制Pten+/-小鼠的肿瘤发展。基因发展2006；20： 1569-74.CAS

PubMed

PubMed

PubMed Central

公共医学中心

Google Scholar

谷歌学者

Grasso CS, Wu YM, Robinson DR, Cao X, Dhanasekaran SM, Khan AP, et al. The mutational landscape of lethal castration-resistant prostate cancer. Nature. 2012;487:239–43.CAS

Grasso CS，Wu YM，Robinson DR，Cao X，Dhanasekaran SM，Khan AP等。致命去势抵抗性前列腺癌的突变景观。自然。2012年；487:239-43.CAS

PubMed

PubMed

PubMed Central

公共医学中心

Google Scholar

谷歌学者

Choi SYC, Ettinger SL, Lin D, Xue H, Ci X, Nabavi N, et al. Targeting MCT4 to reduce lactic acid secretion and glycolysis for treatment of neuroendocrine prostate cancer. Cancer Med. 2018;7:3385–92.CAS

Choi SYC，Ettinger SL，Lin D，Xue H，Ci X，Nabavi N等。靶向MCT4以减少乳酸分泌和糖酵解治疗神经内分泌前列腺癌。癌症医学2018；7： 3385–92.CAS

PubMed

PubMed

PubMed Central

公共医学中心

Google Scholar

谷歌学者

Porporato PE, Filigheddu N, Pedro JMB-S, Kroemer G, Galluzzi L. Mitochondrial metabolism and cancer. Cell Res. 2018;28:265–80.CAS

Porporato PE，Filigheddu N，Pedro JMB-S，Kroemer G，Galluzzi L.线粒体代谢和癌症。Cell Res.2018；

PubMed

PubMed

Google Scholar

谷歌学者

Jia D, Lu M, Jung KH, Park JH, Yu L, Onuchic JN, et al. Elucidating cancer metabolic plasticity by coupling gene regulation with metabolic pathways. Proc Natl Acad Sci USA. 2019;116:3909–18.CAS

Jia D，Lu M，Jung KH，Park JH，Yu L，Onuchic JN等。通过将基因调控与代谢途径相结合来阐明癌症代谢可塑性。美国国家科学院院刊2019；116:3909-18.CAS

PubMed

PubMed

PubMed Central

公共医学中心

Google Scholar

谷歌学者

Cassim S, Vučetić M, Ždralević M, Pouyssegur J. Warburg and beyond: the power of mitochondrial metabolism to collaborate or replace fermentative glycolysis in cancer. Cancers (Basel). 2020;12:1119.CAS

Cassim S，VučetićM，ŽdralevićM，Pouyssegur J.Warburg及其他：线粒体代谢在癌症中协同或替代发酵糖酵解的能力。癌症（巴塞尔）。2020年；12： 1119.CAS

PubMed

PubMed

Google Scholar

谷歌学者

Grasso D, Zampieri LX, Capelôa T, Van de Velde JA, Sonveaux P. Mitochondria in cancer. Cell Stress. 2020;4:114–46.CAS

Grasso D，Zampieri LX，Capelôa T，Van de Velde JA，Sonveaux P.癌症中的线粒体。细胞应激。2020年；4： 114–46.CAS

PubMed

PubMed

PubMed Central

公共医学中心

Google Scholar

谷歌学者

Roth KG, Mambetsariev I, Kulkarni P, Salgia R. The mitochondrion as an emerging therapeutic target in cancer. Trends Mol Med. 2020;26:119–34.CAS

Roth KG，Mambetsariev I，Kulkarni P，Salgia R.线粒体作为癌症新兴治疗靶点。趋势Mol Med。2020；26:119–34.CAS

PubMed

PubMed

Google Scholar

谷歌学者

Mosier JA, Schwager SC, Boyajian DA, Reinhart-King CA. Cancer cell metabolic plasticity in migration and metastasis. Clin Exp Metastasis. 2021;38:343–59.CAS

Mosier JA，Schwager SC，Boyajian DA，Reinhart King CA。迁移和转移中的癌细胞代谢可塑性。临床试验转移。2021年；38:343-59.CAS

PubMed

PubMed

Google Scholar

谷歌学者

Tan YQ, Zhang X, Zhang S, Zhu T, Garg M, Lobie PE, et al. Mitochondria: the metabolic switch of cellular oncogenic transformation. Biochim Biophys Acta Rev Cancer. 2021;1876:188534.CAS

Tan YQ，Zhang X，Zhang S，Zhu T，Garg M，Lobie PE等。线粒体：细胞致癌转化的代谢转换。Biochim Biophys Acta Rev癌症。2021年；1876:188534.CAS

PubMed

PubMed

Google Scholar

谷歌学者

Zhang X, Su Q, Zhou J, Yang Z, Liu Z, Ji L, et al. To betray or to fight? The dual identity of the mitochondria in cancer. Future Oncol. 2021;17:723–43.CAS

张X，苏Q，周J，杨Z，刘Z，季L等。背叛还是斗争？线粒体在癌症中的双重身份。未来Oncol。2021年；17： 723–43.CAS

PubMed

PubMed

Google Scholar

谷歌学者

Uo T, Ojo KK, Sprenger CCT, Soriano Epilepsia K, Perera BGK, Damodarasamy, M et al. A Compound that Inhibits Glycolysis in Prostate Cancer Controls Growth of Advanced Prostate Cancer. Mol Cancer Ther. 2024; https://doi.org/10.1158/1535-7163.MCT-23-0540.Bartman CR, Weilandt DR, Shen Y, Lee WD, Han Y, TeSlaa T, et al.

Uo T，Ojo KK，Sprenger CCT，Soriano Epilepsia K，Perera BGK，Damodarasamy，M等人。一种抑制前列腺癌糖酵解的化合物可控制晚期前列腺癌的生长。摩尔癌症治疗。2024年；https://doi.org/10.1158/1535-7163.MCT-23-0540.BartmanCR，Weilandt博士，Shen Y，Lee WD，Han Y，TeSlaa T等。

Slow TCA flux and ATP production in primary solid tumours but not metastases. Nature. 2023;614:349–57.CAS .

原发性实体瘤中TCA通量和ATP产生缓慢，但不转移。自然。2023年；614:349-57。CAS。

PubMed

PubMed

PubMed Central

公共医学中心

Google Scholar

谷歌学者

Fischer GM, Jalali A, Kircher DA, Lee W-C, McQuade JL, Haydu LE, et al. Molecular profiling reveals unique immune and metabolic features of melanoma brain metastases. Cancer Discov. 2019;9:628–45.CAS

Fischer GM，Jalali A，Kircher DA，Lee W-C，McQuade JL，Haydu LE等。分子谱分析揭示了黑色素瘤脑转移的独特免疫和代谢特征。癌症发现。2019年；9： 628–45.CAS

PubMed

PubMed

PubMed Central

公共医学中心

Google Scholar

谷歌学者

Yap TA, Daver N, Mahendra M, Zhang J, Kamiya-Matsuoka C, Meric-Bernstam F, et al. Complex I inhibitor of oxidative phosphorylation in advanced solid tumors and acute myeloid leukemia: phase I trials. Nat Med. 2023;29:115–26.CAS

Yap TA，Daver N，Mahendra M，Zhang J，Kamiya Matsuoka C，Meric Bernstam F等。晚期实体瘤和急性髓细胞白血病中氧化磷酸化的复合物I抑制剂：I期临床试验。Nat Med。2023；29:115–26.CAS

PubMed

PubMed

Google Scholar

谷歌学者

Mullen AR, Hu Z, Shi X, Jiang L, Boroughs LK, Kovacs Z, et al. Oxidation of alpha-ketoglutarate is required for reductive carboxylation in cancer cells with mitochondrial defects. Cell Rep. 2014;7:1679–90.CAS

Mullen AR，Hu Z，Shi X，Jiang L，Boroughs LK，Kovacs Z等。α-酮戊二酸的氧化是线粒体缺陷癌细胞还原羧化所必需的。Cell Rep.2014；7： 1679-90.CAS

PubMed

PubMed

PubMed Central

公共医学中心

Google Scholar

谷歌学者

Tomlinson IPM, Alam NA, Rowan AJ, Barclay E, Jaeger EEM, Kelsell D, et al. Germline mutations in FH predispose to dominantly inherited uterine fibroids, skin leiomyomata and papillary renal cell cancer. Nat Genet. 2002;30:406–10.CAS

Tomlinson IPM，Alam NA，Rowan AJ，Barclay E，Jaeger EEM，Kelsell D等。FH中的种系突变易患显性遗传的子宫肌瘤，皮肤平滑肌瘤和乳头状肾细胞癌。纳特·吉内特。2002年；30:406–10.CAS

PubMed

PubMed

Google Scholar

谷歌学者

Baysal BE, Ferrell RE, Willett-Brozick JE, Lawrence EC, Myssiorek D, Bosch A, et al. Mutations in SDHD, a mitochondrial complex II gene, in hereditary paraganglioma. Science. 2000;287:848–51.CAS

Baysal BE，Ferrell RE，Willett Brozick JE，Lawrence EC，Myssiorek D，Bosch A等。遗传性副神经节瘤中线粒体复合体II基因SDHD的突变。科学。2000年；287:848-51.CAS

PubMed

PubMed

Google Scholar

谷歌学者

Mullen AR, Wheaton WW, Jin ES, Chen P-H, Sullivan LB, Cheng T, et al. Reductive carboxylation supports growth in tumour cells with defective mitochondria. Nature. 2011;481:385–8.PubMed

Mullen AR，Wheaton WW，Jin ES，Chen P-H，Sullivan LB，Cheng T等。还原羧化支持线粒体缺陷的肿瘤细胞生长。自然。2011年；481:385–8.PubMed

PubMed Central

公共医学中心

Google Scholar

谷歌学者

Astuti D, Latif F, Dallol A, Dahia PL, Douglas F, George E, et al. Gene mutations in the succinate dehydrogenase subunit SDHB cause susceptibility to familial pheochromocytoma and to familial paraganglioma. Am J Hum Genet. 2001;69:49–54.CAS

。我是J Hum Genet。2001年；69:49–54.CAS

PubMed

PubMed

PubMed Central

公共医学中心

Google Scholar

谷歌学者

Killian JK, Kim SY, Miettinen M, Smith C, Merino M, Tsokos M, et al. Succinate dehydrogenase mutation underlies global epigenomic divergence in gastrointestinal stromal tumor. Cancer Discov. 2013;3:648–57.CAS

Killian JK，Kim SY，Miettinen M，Smith C，Merino M，Tsokos M等。琥珀酸脱氢酶突变是胃肠道间质瘤全球表观基因组差异的基础。癌症发现。2013年；3： 648–57.CAS

PubMed

PubMed

PubMed Central

公共医学中心

Google Scholar

谷歌学者

Niemann S, Müller U. Mutations in SDHC cause autosomal dominant paraganglioma, type 3. Nat Genet. 2000;26:268–70.CAS

Niemann S，Müller U.SDHC突变导致常染色体显性副神经节瘤3型。纳特·吉内特。2000年；26:268–70.CAS

PubMed

PubMed

Google Scholar

谷歌学者

Arnold PK, Jackson BT, Paras KI, Brunner JS, Hart ML, Newsom OJ, et al. A non-canonical tricarboxylic acid cycle underlies cellular identity. Nature. 2022;603:477–81.CAS

Arnold PK，Jackson BT，Paras KI，Brunner JS，Hart ML，Newsom OJ等。非经典三羧酸循环是细胞身份的基础。自然。2022年；603:477–81.CAS

PubMed

PubMed

PubMed Central

公共医学中心

Google Scholar

谷歌学者

Cutruzzolà F, Giardina G, Marani M, Macone A, Paiardini A, Rinaldo S, et al. Glucose metabolism in the progression of prostate cancer. Front Physiol. 2017;8:97.PubMed

CutruzzolàF，Giardina G，Marani M，Macone A，Paiardini A，Rinaldo S等。前列腺癌进展中的葡萄糖代谢。前沿生理学。2017年；8： 97.PubMed

PubMed Central

公共医学中心

Google Scholar

谷歌学者

Costello LC, Franklin RB. Citrate metabolism of normal and malignant prostate epithelial cells. Urology. 1997;50:3–12.CAS

科斯特洛LC，富兰克林RB。。泌尿外科。1997年；50:3–12.CAS

PubMed

PubMed

Google Scholar

谷歌学者

Costello LC, Franklin RB. The clinical relevance of the metabolism of prostate cancer; zinc and tumor suppression: connecting the dots. Mol Cancer. 2006;5:17.PubMed

科斯特洛LC，富兰克林RB。前列腺癌代谢的临床相关性；锌与肿瘤抑制：连接点。摩尔癌症。；5： 17.PubMed

PubMed Central

公共医学中心

Google Scholar

谷歌学者

Costello LC, Feng P, Milon B, Tan M, Franklin RB. Role of zinc in the pathogenesis and treatment of prostate cancer: critical issues to resolve. Prostate Cancer Prostatic Dis. 2004;7:111–7.CAS

。锌在前列腺癌发病机制和治疗中的作用：需要解决的关键问题。前列腺癌前列腺疾病。2004年；7： 111–7.CAS

PubMed

PubMed

PubMed Central

公共医学中心

Google Scholar

谷歌学者

Cooper JF, Farid I. The role of citric acid in the physiology of the prostate. 3. Lactate/citrate ratios in benign and malignant prostatic homogenates as an index of prostatic malignancy. J Urol. 1964;92:533–6.CAS

Cooper JF，Farid I.柠檬酸在前列腺生理中的作用。良性和恶性前列腺匀浆中的乳酸/柠檬酸盐比率作为前列腺恶性肿瘤的指标。J乌拉尔。1964年；92:533–6.CAS

PubMed

PubMed

Google Scholar

谷歌学者

Giafaglione JM, Crowell PD, Delcourt AML, Hashimoto T, Ha SM, Atmakuri A, et al. Prostate lineage-specific metabolism governs luminal differentiation and response to antiandrogen treatment. Nat Cell Biol. 2023;25:1821–32.CAS

Giafaglione JM，Crowell PD，Delcourt AML，Hashimoto T，Ha SM，Atmakuri A等。前列腺谱系特异性代谢控制腔内分化和对抗雄激素治疗的反应。Nat细胞生物学。2023年；25:1821-32.CAS

PubMed

PubMed

PubMed Central

公共医学中心

Google Scholar

谷歌学者

Costello LC, Franklin RB, Feng P. Mitochondrial function, zinc, and intermediary metabolism relationships in normal prostate and prostate cancer. Mitochondrion. 2005;5:143–53.CAS

Costello LC，Franklin RB，Feng P.正常前列腺癌和前列腺癌中的线粒体功能，锌和中间代谢关系。线粒体。2005年；5： 143–53.CAS

PubMed

PubMed

PubMed Central

公共医学中心

Google Scholar

谷歌学者

Frégeau-Proulx L, Lacouture A, Berthiaume L, Weidmann C, Harvey M, Gonthier K, et al. Multiple metabolic pathways fuel the truncated tricarboxylic acid cycle of the prostate to sustain constant citrate production and secretion. Mol Metab. 2022;62:101516.PubMed

Frégeau Proulx L，Lacouture A，Berthiaume L，Weidmann C，Harvey M，Gonthier K等。多种代谢途径促进前列腺的截短三羧酸循环，以维持恒定的柠檬酸盐产生和分泌。摩尔代谢。2022年；62:101516.PubMed

PubMed Central

公共医学中心

Google Scholar

谷歌学者

Zou J, Milon BC, Desouki MM, Costello LC, Franklin RB. hZIP1 zinc transporter down-regulation in prostate cancer involves the overexpression of ras responsive element binding protein-1 (RREB-1). Prostate. 2011;71:1518–24.CAS

邹J，米隆BC，德苏基MM，科斯特洛LC，富兰克林RB。前列腺癌中hZIP1锌转运蛋白的下调涉及ras反应元件结合蛋白-1（RREB-1）的过表达。前列腺。2011年；71:1518-24.CAS

PubMed

PubMed

PubMed Central

公共医学中心

Google Scholar

谷歌学者

Milon BC, Agyapong A, Bautista R, Costello LC, Franklin RB. Ras responsive element binding protein-1 (RREB-1) down-regulates hZIP1 expression in prostate cancer cells. Prostate. 2010;70:288–96.CAS

米隆BC，Agyapong A，Bautista R，Costello LC，Franklin RB。Ras反应元件结合蛋白-1（RREB-1）下调前列腺癌细胞中hZIP1的表达。前列腺。2010年；70:288–96.CAS

PubMed

PubMed

PubMed Central

公共医学中心

Google Scholar

谷歌学者

Shao Y, Ye G, Ren S, Piao H-L, Zhao X, Lu X, et al. Metabolomics and transcriptomics profiles reveal the dysregulation of the tricarboxylic acid cycle and related mechanisms in prostate cancer. Int J Cancer. 2018;143:396–407.CAS

。Int J癌症。2018年；143:396-407.CAS

PubMed

PubMed

Google Scholar

谷歌学者

Ahmad F, Cherukuri MK, Choyke PL. Metabolic reprogramming in prostate cancer. Br J Cancer. 2021;125:1185–96.PubMed

Ahmad F，Cherukuri MK，Choyke PL.前列腺癌中的代谢重编程。Br J癌症。2021年；125:1185–96.PubMed

PubMed Central

公共医学中心

Google Scholar

谷歌学者

Mahmood M, Liu EM, Shergold AL, Tolla E, Tait-Mulder J, Huerta-Uribe A, et al. Mitochondrial DNA mutations drive aerobic glycolysis to enhance checkpoint blockade response in melanoma. Nat Cancer. 2024. https://doi.org/10.1038/s43018-023-00721-w.Wheaton WW, Weinberg SE, Hamanaka RB, Soberanes S, Sullivan LB, Anso E, et al.

Mahmood M，Liu EM，Shergold AL，Tolla E，Tait Mulder J，Huerta Uribe A等。线粒体DNA突变驱动有氧糖酵解以增强黑色素瘤的检查点阻断反应。Nat癌症。2024https://doi.org/10.1038/s43018-023-00721-w.Wheaton。

Metformin inhibits mitochondrial complex I of cancer cells to reduce tumorigenesis. Elife. 2014;3:e02242.PubMed .

二甲双胍抑制癌细胞的线粒体复合物I以减少肿瘤发生。埃利夫。2014年；3： e02242。PubMed。

PubMed Central

公共医学中心

Google Scholar

谷歌学者

Heinz S, Freyberger A, Lawrenz B, Schladt L, Schmuck G, Ellinger-Ziegelbauer H. Mechanistic investigations of the mitochondrial complex I inhibitor rotenone in the context of pharmacological and safety evaluation. Sci Rep. 2017;7:45465.CAS

Heinz S，Freyberger A，Lawrenz B，Schladt L，Schmuck G，Ellinger Ziegelbauer H.在药理学和安全性评估的背景下对线粒体复合物I抑制剂鱼藤酮的机理研究。Sci代表2017；7：

PubMed

PubMed

PubMed Central

公共医学中心

Google Scholar

谷歌学者

Zaidi S, Gandhi J, Joshi G, Smith NL, Khan SA. The anticancer potential of metformin on prostate cancer. Prostate Cancer Prostatic Dis. 2019;22:351–61.PubMed

Zaidi S，Gandhi J，Joshi G，Smith NL，Khan SA。二甲双胍对前列腺癌的抗癌潜力。前列腺癌前列腺疾病。2019年；22:351–61.PubMed

Google Scholar

谷歌学者

Naguib A, Mathew G, Reczek CR, Watrud K, Ambrico A, Herzka T, et al. Mitochondrial complex I inhibitors expose a vulnerability for selective killing of Pten-null cells. Cell Rep. 2018;23:58–67.CAS

Naguib A，Mathew G，Reczek CR，Watrud K，Ambrico A，Herzka T等。线粒体复合物I抑制剂暴露出选择性杀死Pten无效细胞的脆弱性。细胞代表2018；23:58–67.CAS

PubMed

PubMed

PubMed Central

公共医学中心

Google Scholar

谷歌学者

Bader DA, McGuire SE. Tumour metabolism and its unique properties in prostate adenocarcinoma. Nat Rev Urol. 2020;17:214–31.PubMed

Bader DA，McGuire SE。前列腺癌中的肿瘤代谢及其独特性质。Nat Rev Urol。2020年；17： 214-31.PubMed

Google Scholar

谷歌学者

Bader DA, Hartig SM, Putluri V, Foley C, Hamilton MP, Smith EA, et al. Mitochondrial pyruvate import is a metabolic vulnerability in androgen receptor-driven prostate cancer. Nat Metab. 2019;1:70–85.CAS

Bader DA，Hartig SM，Putluri V，Foley C，Hamilton MP，Smith EA等。线粒体丙酮酸输入是雄激素受体驱动的前列腺癌的代谢脆弱性。自然代谢。2019年；1： 70–85.CAS

PubMed

PubMed

Google Scholar

谷歌学者

Patra KC, Hay N. The pentose phosphate pathway and cancer. Trends Biochem Sci. 2014;39:347–54.CAS

Patra KC，Hay N.戊糖磷酸途径与癌症。。2014年；39:347-54.CAS

PubMed

PubMed

PubMed Central

公共医学中心

Google Scholar

谷歌学者

Jin L, Zhou Y. Crucial role of the pentose phosphate pathway in malignant tumors. Oncol Lett. 2019;17:4213–21.CAS

Jin L，Zhou Y.戊糖磷酸途径在恶性肿瘤中的关键作用。Oncol Lett。2019年；17： 4213–21.CAS

PubMed

PubMed

PubMed Central

公共医学中心

Google Scholar

谷歌学者

Ronquist G, Theodorsson E. Inherited, non-spherocytic haemolysis due to deficiency of glucose-6-phosphate dehydrogenase. Scand J Clin Lab Invest. 2007;67:105–11.CAS

Ronquist G，Theodorsson E.由于缺乏葡萄糖-6-磷酸脱氢酶而遗传性非球形溶血。Scand J Clin实验室投资。2007年；67:105–11.CAS

PubMed

PubMed

Google Scholar

谷歌学者

Mehta A, Mason PJ, Vulliamy TJ. Glucose-6-phosphate dehydrogenase deficiency. Baillieres Best Pr Res Clin Haematol. 2000;13:21–38.CAS

Mehta A，Mason PJ，Vulliamy TJ。葡萄糖-6-磷酸脱氢酶缺乏症。Bailliers Best Pr Res Clin Haematol公司。2000年；13： 21-38.CAS

Google Scholar

谷歌学者

Cappellini MD, Fiorelli G. Glucose-6-phosphate dehydrogenase deficiency. Lancet. 2008;371:64–74.CAS

Cappellini MD，Fiorelli G.葡萄糖-6-磷酸脱氢酶缺乏症。柳叶刀。2008年；371:64-74.CAS

PubMed

PubMed

Google Scholar

谷歌学者

Dore MP, Davoli A, Longo N, Marras G, Pes GM. Glucose-6-phosphate dehydrogenase deficiency and risk of colorectal cancer in Northern Sardinia: a retrospective observational study. Medicine. 2016;95:e5254.PubMed

。医学。；95:e5254.PubMed

PubMed Central

公共医学中心

Google Scholar

谷歌学者

Kowalik MA, Columbano A, Perra A. Emerging role of the pentose phosphate pathway in hepatocellular carcinoma. Front Oncol. 2017;7:87.PubMed

Kowalik MA，Columbano A，Perra A.戊糖磷酸途径在肝细胞癌中的新兴作用。前部Oncol。2017年；7： 87.PubMed

PubMed Central

公共医学中心

Google Scholar

谷歌学者

Chen M, Shen M, Li Y, Liu C, Zhou K, Hu W, et al. GC-MS-based metabolomic analysis of human papillary thyroid carcinoma tissue. Int J Mol Med. 2015;36:1607–14.PubMed

陈敏，沈敏，李毅，刘超，周凯，胡伟，等。基于GC-MS的人甲状腺乳头状癌组织代谢组学分析。Int J Mol Med。2015；36:1607–14.PubMed

Google Scholar

谷歌学者

Cohen HJ, Elizalde A, Miller SP. Cytologic studies of glucose-6-phosphate dehydrogenase in malignancy. Cancer. 1968;21:1055–60.CAS

Cohen HJ，Elizalde A，Miller SP。恶性肿瘤中葡萄糖-6-磷酸脱氢酶的细胞学研究。癌症。1968年；21:1055-60.CAS

PubMed

PubMed

Google Scholar

谷歌学者

Langbein S, Frederiks WM, zur Hausen A, Popa J, Lehmann J, Weiss C, et al. Metastasis is promoted by a bioenergetic switch: new targets for progressive renal cell cancer. Int J Cancer. 2008;122:2422–8.CAS

Langbein S，Frederiks WM，zur Hausen A，Popa J，Lehmann J，Weiss C等。生物能量转换促进转移：进行性肾细胞癌的新靶点。Int J癌症。2008年；122:2422–8.CAS

PubMed

PubMed

Google Scholar

谷歌学者

Lu M, Lu L, Dong Q, Yu G, Chen J, Qin L, et al. Elevated G6PD expression contributes to migration and invasion of hepatocellular carcinoma cells by inducing epithelial-mesenchymal transition. Acta Biochim Biophys Sin (Shanghai). 2018;50:370–80.CAS

Lu M，Lu L，Dong Q，Yu G，Chen J，Qin L等。G6PD表达升高通过诱导上皮-间质转化促进肝细胞癌细胞的迁移和侵袭。生物化学学报（上海）。2018年；50:370–80.CAS

PubMed

PubMed

Google Scholar

谷歌学者

Dong T, Kang X, Liu Z, Zhao S, Ma W, Xuan Q, et al. Altered glycometabolism affects both clinical features and prognosis of triple-negative and neoadjuvant chemotherapy-treated breast cancer. Tumour Biol. 2016;37:8159–68.CAS

Dong T，Kang X，Liu Z，Zhao S，Ma W，Xuan Q，et al。糖代谢改变影响三阴性和新辅助化疗治疗乳腺癌的临床特征和预后。肿瘤生物学。；37:8159–68.CAS

PubMed

PubMed

Google Scholar

谷歌学者

Pu H, Zhang Q, Zhao C, Shi L, Wang Y, Wang J, et al. Overexpression of G6PD is associated with high risks of recurrent metastasis and poor progression-free survival in primary breast carcinoma. World J Surg Oncol. 2015;13:323.PubMed

Pu H，Zhang Q，Zhao C，Shi L，Wang Y，Wang J，et al。G6PD的过度表达与原发性乳腺癌复发转移的高风险和无进展生存率低有关。世界J Surg Oncol。2015年；13： 323.PubMed

PubMed Central

公共医学中心

Google Scholar

谷歌学者

Zampella EJ, Bradley ELJ, Pretlow TG 2nd. Glucose-6-phosphate dehydrogenase: a possible clinical indicator for prostatic carcinoma. Cancer. 1982;49:384–7.CAS

Zampella EJ，Bradley ELJ，Pretlow TG第二。葡萄糖-6-磷酸脱氢酶：前列腺癌的可能临床指标。癌症。1982年；49:384–7.CAS

PubMed

PubMed

Google Scholar

谷歌学者

Tsouko E, Khan AS, White MA, Han JJ, Shi Y, Merchant FA, et al. Regulation of the pentose phosphate pathway by an androgen receptor-mTOR-mediated mechanism and its role in prostate cancer cell growth. Oncogenesis. 2014;3:e103.CAS

Tsouko E，Khan AS，White MA，Han JJ，Shi Y，Merchant FA等。雄激素受体mTOR介导的机制对磷酸戊糖途径的调节及其在前列腺癌细胞生长中的作用。肿瘤发生。2014年；3： e103.CAS

PubMed

PubMed

PubMed Central

公共医学中心

Google Scholar

谷歌学者

Whitburn J, Rao SR, Morris EV, Tabata S, Hirayama A, Soga T, et al. Metabolic profiling of prostate cancer in skeletal microenvironments identifies G6PD as a key mediator of growth and survival. Sci Adv. 2022;8:eabf9096.CAS

Whitburn J，Rao SR，Morris EV，Tabata S，Hirayama A，Soga T等。骨骼微环境中前列腺癌的代谢谱确定G6PD是生长和存活的关键介质。Sci Adv.2022；8： eabf9096.CAS

PubMed

PubMed

PubMed Central

公共医学中心

Google Scholar

谷歌学者

Gillis JL, Hinneh JA, Ryan NK, Irani S, Moldovan M, Quek L-E, et al. A feedback loop between the androgen receptor and 6-phosphogluoconate dehydrogenase (6PGD) drives prostate cancer growth. Elife. 2021;10:e62592.CAS

Gillis JL，Hinneh JA，Ryan NK，Irani S，Moldovan M，Quek L-E等。雄激素受体和6-磷酸葡萄糖酸脱氢酶（6PGD）之间的反馈回路驱动前列腺癌的生长。埃利夫。2021年；10： e62592.CAS

PubMed

PubMed

PubMed Central

公共医学中心

Google Scholar

谷歌学者

Marshall S, Bacote V, Traxinger RR. Discovery of a metabolic pathway mediating glucose-induced desensitization of the glucose transport system. Role hexosamine biosynth induction insulin resistance. J Biol Chem. 1991;266:4706–12.CAS

Marshall S，Bacote V，Traxinger RR。发现介导葡萄糖诱导的葡萄糖转运系统脱敏的代谢途径。己糖胺生物合成诱导胰岛素抵抗的作用。生物化学杂志。1991年；266:4706–12.CAS

PubMed

PubMed

Google Scholar

谷歌学者

Ying H, Kimmelman AC, Lyssiotis CA, Hua S, Chu GC, Fletcher-Sananikone E, et al. Oncogenic Kras maintains pancreatic tumors through regulation of anabolic glucose metabolism. Cell. 2012;149:656–70.CAS

Ying H，Kimmelman AC，Lyssiotis CA，Hua S，Chu GC，Fletcher-Sananikone E等。致癌Kras通过调节合成代谢葡萄糖代谢来维持胰腺肿瘤。细胞。2012年；149:656–70.CAS

PubMed

PubMed

PubMed Central

公共医学中心

Google Scholar

谷歌学者

Moloughney JG, Kim PK, Vega-Cotto NM, Wu C-C, Zhang S, Adlam M, et al. mTORC2 responds to glutamine catabolite levels to modulate the hexosamine biosynthesis enzyme GFAT1. Mol Cell. 2016;63:811–26.CAS

Moloughney JG，Kim PK，Vega Cotto NM，Wu C-C，Zhang S，Adlam M等。mTORC2响应谷氨酰胺分解代谢产物水平以调节己糖胺生物合成酶GFAT1。摩尔细胞。；63:811-26.CAS

PubMed

PubMed

PubMed Central

公共医学中心

Google Scholar

谷歌学者

Moloughney JG, Vega-Cotto NM, Liu S, Patel C, Kim PK, Wu C-C, et al. mTORC2 modulates the amplitude and duration of GFAT1 Ser-243 phosphorylation to maintain flux through the hexosamine pathway during starvation. J Biol Chem. 2018;293:16464–78.CAS

Moloughney JG，Vega Cotto NM，Liu S，Patel C，Kim PK，Wu C-C等。mTORC2调节GFAT1 Ser-243磷酸化的幅度和持续时间，以维持饥饿期间通过己糖胺途径的通量。生物化学杂志。2018年；293:16464-78.CAS

PubMed

PubMed

PubMed Central

公共医学中心

Google Scholar

谷歌学者

Lucena MC, Carvalho-Cruz P, Donadio JL, Oliveira IA, de Queiroz RM, Marinho-Carvalho MM, et al. Epithelial mesenchymal transition induces aberrant glycosylation through hexosamine biosynthetic pathway activation. J Biol Chem. 2016;291:12917–29.CAS

Lucena MC，Carvalho Cruz P，Donadio JL，Oliveira IA，de Queiroz RM，Marinho Carvalho MM等。上皮-间质转化通过己糖胺生物合成途径激活诱导异常糖基化。生物化学杂志。；291:12917–29.CAS

PubMed

PubMed

PubMed Central

公共医学中心

Google Scholar

谷歌学者

Caldwell SA, Jackson SR, Shahriari KS, Lynch TP, Sethi G, Walker S, et al. Nutrient sensor O-GlcNAc transferase regulates breast cancer tumorigenesis through targeting of the oncogenic transcription factor FoxM1. Oncogene. 2010;29:2831–42.CAS

Caldwell SA，Jackson SR，Shahriari KS，Lynch TP，Sethi G，Walker S等。营养传感器O-GlcNAc转移酶通过靶向致癌转录因子FoxM1来调节乳腺癌的发生。致癌基因。2010年；29:2831-42.CAS

PubMed

PubMed

Google Scholar

谷歌学者

Champattanachai V, Netsirisawan P, Chaiyawat P, Phueaouan T, Charoenwattanasatien R, Chokchaichamnankit D, et al. Proteomic analysis and abrogated expression of O-GlcNAcylated proteins associated with primary breast cancer. Proteomics. 2013;13:2088–99.CAS

Champattanachai V，Netsirisawan P，Chaiyawat P，Phueaouan T，Charoenwattanasatien R，Chokchaichamnankit D等。蛋白质组学分析和废除与原发性乳腺癌相关的O-GlcNAcylated蛋白的表达。。2013年；13： 2088–99.CAS

PubMed

PubMed

Google Scholar

谷歌学者

Mi W, Gu Y, Han C, Liu H, Fan Q, Zhang X, et al. O-GlcNAcylation is a novel regulator of lung and colon cancer malignancy. Biochim Biophys Acta. 2011;1812:514–9.CAS

Mi W，Gu Y，Han C，Liu H，Fan Q，Zhang X等。O-GlcNAcylation是肺癌和结肠癌恶性肿瘤的新型调节剂。生物化学生物物理学报。2011年；1812:514-9.CAS

PubMed

PubMed

Google Scholar

谷歌学者

Zhu Q, Zhou L, Yang Z, Lai M, Xie H, Wu L, et al. O-GlcNAcylation plays a role in tumor recurrence of hepatocellular carcinoma following liver transplantation. Med Oncol. 2012;29:985–93.CAS

Zhu Q，Zhou L，Yang Z，Lai M，Xie H，Wu L等。O-GlcNAcylation在肝移植后肝细胞癌的肿瘤复发中起作用。医学Oncol。2012年；29:985-93.CAS

PubMed

PubMed

Google Scholar

谷歌学者

Krześlak A, Wójcik-Krowiranda K, Forma E, Bieńkiewicz A, Bryś M. Expression of genes encoding for enzymes associated with O-GlcNAcylation in endometrial carcinomas: clinicopathologic correlations. Ginekol Pol. 2012;83:22–26.PubMed

Krześlak A，Wójcik Krowiranda K，Forma E，Bieńkiewicz A，Bry \347 M。子宫内膜癌中编码O-GlcNAcylation相关酶的基因表达：临床病理相关性。Ginekol Pol。2012;83:22–26.PubMed

Google Scholar

谷歌学者

Kim MJ, Choi MY, Lee DH, Roh GS, Kim HJ, Kang SS, et al. O-linked N-acetylglucosamine transferase enhances secretory clusterin expression via liver X receptors and sterol response element binding protein regulation in cervical cancer. Oncotarget. 2018;9:4625–36.PubMed

Kim MJ，Choi MY，Lee DH，Roh GS，Kim HJ，Kang SS等。O-连接的N-乙酰葡糖胺转移酶通过肝X受体和固醇反应元件结合蛋白调节增强宫颈癌中分泌性聚集蛋白的表达。Oncotarget。2018年；9： 4625–36.PubMed

Google Scholar

谷歌学者

Ma Z, Vocadlo DJ, Vosseller K. Hyper-O-GlcNAcylation is anti-apoptotic and maintains constitutive NF-κB activity in pancreatic cancer cells. J Biol Chem. 2013;288:15121–30.CAS

Ma Z，Vocadlo DJ，Vosseller K.Hyper-O-GlcNAcylation具有抗凋亡作用，并在胰腺癌细胞中维持组成型NF-κB活性。生物化学杂志。2013年；288:15121–30.CAS

PubMed

PubMed

PubMed Central

公共医学中心

Google Scholar

谷歌学者

Itkonen HM, Minner S, Guldvik IJ, Sandmann MJ, Tsourlakis MC, Berge V, et al. O-GlcNAc transferase integrates metabolic pathways to regulate the stability of c-MYC in human prostate cancer cells. Cancer Res. 2013;73:5277–87.CAS

Itkonen HM，Minner S，Guldvik IJ，Sandmann MJ，Tsourlakis MC，Berge V等。O-GlcNAc转移酶整合代谢途径以调节人前列腺癌细胞中c-MYC的稳定性。癌症研究2013；73:5277–87.CAS

PubMed

PubMed

Google Scholar

谷歌学者

Munkley J, Vodak D, Livermore KE, James K, Wilson BT, Knight B, et al. Glycosylation is an androgen-regulated process essential for prostate cancer cell viability. EBioMedicine. 2016;8:103–16.PubMed

Munkley J，Vodak D，Livermore KE，James K，Wilson BT，Knight B等。糖基化是雄激素调节的过程，对前列腺癌细胞活力至关重要。EBioMedicine。；8： 103-16.PubMed

PubMed Central

公共医学中心

Google Scholar

谷歌学者

Albitar M, Ma W, Lund L, Albitar F, Diep K, Fritsche HA, et al. Predicting prostate biopsy results using a panel of plasma and urine biomarkers combined in a scoring system. J Cancer. 2016;7:297–303.CAS

Albitar M，Ma W，Lund L，Albitar F，Diep K，Fritsche HA等。使用一组血浆和尿液生物标志物结合评分系统预测前列腺活检结果。J癌症。；7： 297–303.CAS

PubMed

PubMed

PubMed Central

公共医学中心

Google Scholar

谷歌学者

Itkonen HM, Engedal N, Babaie E, Luhr M, Guldvik IJ, Minner S, et al. UAP1 is overexpressed in prostate cancer and is protective against inhibitors of N-linked glycosylation. Oncogene. 2015;34:3744–50.CAS

Itkonen HM，Engedal N，Babaie E，Luhr M，Guldvik IJ，Minner S等。UAP1在前列腺癌中过表达，对N-连接糖基化抑制剂具有保护作用。致癌基因。2015年；34:3744–50.CAS

PubMed

PubMed

Google Scholar

谷歌学者

Scott E, Hodgson K, Calle B, Turner H, Cheung K, Bermudez A, et al. Upregulation of GALNT7 in prostate cancer modifies O-glycosylation and promotes tumour growth. Oncogene. 2023;42:926–37.CAS

Scott E，Hodgson K，Calle B，Turner H，Cheung K，Bermudez A等。GALNT7在前列腺癌中的上调可改变O-糖基化并促进肿瘤生长。致癌基因。2023年；42:926–37.CAS

PubMed

PubMed

PubMed Central

公共医学中心

Google Scholar

谷歌学者

Rossi M, Altea-Manzano P, Demicco M, Doglioni G, Bornes L, Fukano M, et al. PHGDH heterogeneity potentiates cancer cell dissemination and metastasis. Nature. 2022;605:747–53.CAS

Rossi M，Altea Manzano P，Demicco M，Doglioni G，Bornes L，Fukano M等。PHGDH异质性增强癌细胞的传播和转移。自然。2022年；605:747–53.CAS

PubMed

PubMed

PubMed Central

公共医学中心

Google Scholar

谷歌学者

Samaržija I. Post-translational modifications that drive prostate cancer progression. Biomolecules. 2021;11:247.PubMed

Samaržija I.驱动前列腺癌进展的翻译后修饰。生物分子。2021年；11： 247.PubMed

PubMed Central

公共医学中心

Google Scholar

谷歌学者

Itkonen HM, Gorad SS, Duveau DY, Martin SES, Barkovskaya A, Bathen TF, et al. Inhibition of O-GlcNAc transferase activity reprograms prostate cancer cell metabolism. Oncotarget. 2016;7:12464–76.PubMed

Itkonen HM，Gorad SS，Duveau DY，Martin SES，Barkovskaya A，Bathen TF等。抑制O-GlcNAc转移酶活性可重新编程前列腺癌细胞代谢。Oncotarget。；7： 12464–76.PubMed

PubMed Central

公共医学中心

Google Scholar

谷歌学者

de Queiroz RM, Madan R, Chien J, Dias WB, Slawson C. Changes in O-linked N-acetylglucosamine (O-GlcNAc) homeostasis activate the p53 pathway in ovarian cancer cells. J Biol Chem. 2016;291:18897–914.PubMed

de Queiroz RM，Madan R，Chien J，Dias WB，Slawson C.O-连接的N-乙酰葡糖胺（O-GlcNAc）稳态的变化激活卵巢癌细胞中的p53途径。生物化学杂志。；291:18897–914.PubMed

PubMed Central

公共医学中心

Google Scholar

谷歌学者

Kaushik AK, Shojaie A, Panzitt K, Sonavane R, Venghatakrishnan H, Manikkam M, et al. Inhibition of the hexosamine biosynthetic pathway promotes castration-resistant prostate cancer. Nat Commun. 2016;7:11612.CAS

Kaushik AK，Shojaie A，Panzitt K，Sonavane R，Venghatakrishnan H，Manikkam M等。抑制己糖胺生物合成途径可促进去势抵抗性前列腺癌。纳特公社。；7： 11612.CAS

PubMed

PubMed

PubMed Central

公共医学中心

Google Scholar

谷歌学者

Baenke F, Peck B, Miess H, Schulze A. Hooked on fat: the role of lipid synthesis in cancer metabolism and tumour development. Dis Model Mech. 2013;6:1353–63.Broadfield LA, Pane AA, Talebi A, Swinnen JV, Fendt SM. Lipid metabolism in cancer: new perspectives and emerging mechanisms. Dev Cell.

Baenke F，Peck B，Miess H，Schulze A.痴迷于脂肪：脂质合成在癌症代谢和肿瘤发展中的作用。Dis模型机械。2013年；6： 1353-63。Broadfield LA，Pane AA，Talebi A，Swinnen JV，Fendt SM。癌症中的脂质代谢：新观点和新兴机制。开发单元。

2021;56:1363–93.CAS .

2021年；56:1363年至93年。

PubMed

PubMed

Google Scholar

谷歌学者

Giunchi F, Fiorentino M, Loda M. The metabolic landscape of prostate cancer. Eur Urol Oncol. 2019;2:28–36.PubMed

Giunchi F，Fiorentino M，Loda M.前列腺癌的代谢景观。Eur Urol Oncol。2019年；2：

Google Scholar

谷歌学者

Butler LM, Centenera MM, Swinnen JV. Androgen control of lipid metabolism in prostate cancer: novel insights and future applications. Endocr Relat Cancer. 2016;23:R219–27.CAS

巴特勒LM，Centenera MM，Swinnen JV。雄激素控制前列腺癌脂质代谢：新见解和未来应用。内分泌相关癌症。；23:R219-27.CAS

PubMed

PubMed

Google Scholar

谷歌学者

Swinnen JV, Verhoeven G. Androgens and the control of lipid metabolism in human prostate cancer cells. J Steroid Biochem Mol Biol. 1998;65:191–8.CAS

Swinnen JV，Verhoeven G.雄激素和人前列腺癌细胞脂质代谢的控制。J类固醇生物化学分子生物学。1998年；65:191–8.CAS

PubMed

PubMed

Google Scholar

谷歌学者

Pardo JC, de Porras VR, Gil J, Font A, Puig-Domingo M, Jordà M. Lipid metabolism and epigenetics crosstalk in prostate cancer. Nutrients. 2022;14:851.CAS

Pardo JC，de Porras VR，Gil J，Font A，Puig Domingo M，JordàM.前列腺癌中的脂质代谢和表观遗传学串扰。营养素。2022年；14：

PubMed

PubMed

PubMed Central

公共医学中心

Google Scholar

谷歌学者

Lounis MA, Péant B, Leclerc-Desaulniers K, Ganguli D, Daneault C, Ruiz M, et al. Modulation of de novo lipogenesis improves response to enzalutamide treatment in prostate cancer. Cancers (Basel). 2020;12:1–21.

Lounis MA，Péant B，Leclerc Desaulniers K，Ganguli D，Daneault C，Ruiz M等。从头脂肪生成的调节改善了前列腺癌对enzalutamide治疗的反应。癌症（巴塞尔）。2020年；12： 1-21岁。

Google Scholar

谷歌学者

Butler LM, Mah CY, Machiels J, Vincent AD, Irani S, Mutuku SM, et al. Lipidomic profiling of clinical prostate cancer reveals targetable alterations in membrane lipid composition. Cancer Res. 2021;81:4981–93.CAS

Butler LM，Mah CY，Machiels J，Vincent AD，Irani S，Mutuku SM等。临床前列腺癌的脂质组学分析揭示了膜脂质组成的可靶向改变。癌症研究2021；81:4981–93.CAS

PubMed

PubMed

Google Scholar

谷歌学者

Mounier C, Bouraoui L, Rassart E. Lipogenesis in cancer progression (review). Int J Oncol. 2014;45:485–92.CAS

Mounier C，Bouraoui L，Rassart E.癌症进展中的脂肪生成（综述）。国际癌症杂志。2014年；45:485–92.CAS

PubMed

PubMed

Google Scholar

谷歌学者

Huang WC, Li X, Liu J, Lin J, Chung LWK. Activation of androgen receptor, lipogenesis, and oxidative stress converged by SREBP-1 is responsible for regulating growth and progression of prostate cancer cells. Mol Cancer Res. 2012;10:133–42.CAS

黄WC，李X，刘J，林J，钟LWK。SREBP-1聚集的雄激素受体，脂肪生成和氧化应激的激活负责调节前列腺癌细胞的生长和进展。Mol Cancer Res.2012；10： 133–42.CAS

PubMed

PubMed

Google Scholar

谷歌学者

Lee MY, Moon JS, Park SW, Koh YK, Ahn YH, Kim KS. KLF5 enhances SREBP-1 action in androgen-dependent induction of fatty acid synthase in prostate cancer cells. Biochem J. 2009;417:313–22.CAS

Lee MY，Moon JS，Park SW，Koh YK，Ahn YH，Kim KS。KLF5增强SREBP-1在前列腺癌细胞中雄激素依赖性诱导脂肪酸合酶中的作用。生物化学J.2009；417:313-22.CAS

PubMed

PubMed

Google Scholar

谷歌学者

Hamada S, Horiguchi A, Kuroda K, Ito K, Asano T, Miyai K, et al. Increased fatty acid synthase expression in prostate biopsy cores predicts higher Gleason score in radical prostatectomy specimen. BMC Clin Pathol. 2014;14:3.PubMed

Hamada S，Horiguchi A，Kuroda K，Ito K，Asano T，Miyai K等。前列腺活检核心中脂肪酸合酶表达的增加预示着根治性前列腺切除术标本中Gleason评分较高。BMC临床病理学。2014年；14： 3.PubMed

PubMed Central

公共医学中心

Google Scholar

谷歌学者

Bastos DC, Ribeiro CF, Ahearn T, Nascimento J, Pakula H, Clohessy J, et al. Genetic ablation of FASN attenuates the invasive potential of prostate cancer driven by Pten loss. J Pathol. 2021;253:292–303.CAS

Bastos DC，Ribeiro CF，Ahearn T，Nascimento J，Pakula H，Clohessy J等。FASN的基因消融减弱了由Pten丢失驱动的前列腺癌的侵袭潜力。J Pathol。2021年；253:292–303.CAS

PubMed

PubMed

Google Scholar

谷歌学者

Li X, Chen YT, Hu P, Huang WC. Fatostatin displays high antitumor activity in prostate cancer by blocking SREBP-regulated metabolic pathways and androgen receptor signaling. Mol Cancer Ther. 2014;13:855–66.CAS

李X，陈YT，胡P，黄WC。Fatostatin通过阻断SREBP调节的代谢途径和雄激素受体信号传导在前列腺癌中显示出高抗肿瘤活性。摩尔癌症治疗。2014年；13： 855–66.CAS

PubMed

PubMed

PubMed Central

公共医学中心

Google Scholar

谷歌学者

Schmidt LJ, Ballman KV, Tindall DJ. Inhibition of fatty acid synthase activity in prostate cancer cells by dutasteride. Prostate. 2007;67:1111–20.CAS

Schmidt LJ，Ballman KV，Tindall DJ。度他雄胺对前列腺癌细胞脂肪酸合酶活性的抑制作用。前列腺。2007年；67:1111–20.CAS

PubMed

PubMed

Google Scholar

谷歌学者

Rae C, Fragkoulis GI, Chalmers AJ. Cytotoxicity and radiosensitizing activity of the fatty acid synthase inhibitor C75 is enhanced by blocking fatty acid uptake in prostate cancer cells. Adv Radiat Oncol. 2020;5:994–1005.PubMed

Rae C，Fragkoulis GI，Chalmers AJ。脂肪酸合酶抑制剂C75的细胞毒性和放射增敏活性通过阻断前列腺癌细胞中的脂肪酸摄取而增强。Adv Radiat Oncol公司。2020年；5： 994–1005.PubMed

PubMed Central

公共医学中心

Google Scholar

谷歌学者

Chuang HY, Lee YP, Lin WC, Lin YH, Hwang JJ. Fatty acid inhibition sensitizes androgen-dependent and -independent prostate cancer to radiotherapy via FASN/NF-κB pathway. Sci Rep. 2019;9:13284.PubMed

Chuang HY，Lee YP，Lin WC，Lin YH，Hwang JJ。脂肪酸抑制通过FASN/NF-κB途径使雄激素依赖性和非依赖性前列腺癌对放疗敏感。Sci代表2019；9： 13284.PubMed

PubMed Central

公共医学中心

Google Scholar

谷歌学者

Centenera MM, Scott JS, Machiels J, Nassar ZD, Miller DC, Zinonos I, et al. ELOVL5 is a critical and targetable fatty acid elongase in prostate cancer. Cancer Res. 2021;81:1704–18.CAS

Centenera MM，Scott JS，Machiels J，Nassar ZD，Miller DC，Zinoos I等。ELOVL5是前列腺癌中关键且可靶向的脂肪酸延长酶。癌症研究2021；81:1704-18.CAS

PubMed

PubMed

Google Scholar

谷歌学者

Xu H, Li S, Sun Y, Xu L, Hong X, Wang Z, et al. ELOVL5-mediated long chain fatty acid elongation contributes to enzalutamide resistance of prostate cancer. Cancers (Basel). 2021;13:1–12.

Xu H，Li S，Sun Y，Xu L，Hong X，Wang Z等。ELOVL5介导的长链脂肪酸延伸有助于前列腺癌的恩扎鲁胺耐药性。癌症（巴塞尔）。2021年；13： 1–12。

Google Scholar

谷歌学者

Kaini RR, Sillerud LO, Zhaorigetu S, Hu CAA. Autophagy regulates lipolysis and cell survival through lipid droplet degradation in androgen-sensitive prostate cancer cells. Prostate. 2012;72:1412–22.CAS

Kaini RR，Sillerud LO，Zhaorigetu S，Hu CAA。自噬通过雄激素敏感的前列腺癌细胞中的脂滴降解来调节脂解和细胞存活。前列腺。2012年；72:1412-22.CAS

PubMed

PubMed

PubMed Central

公共医学中心

Google Scholar

谷歌学者

Nomura DK, Lombardi DP, Chang JW, Niessen S, Ward AM, Long JZ, et al. Monoacylglycerol lipase exerts dual control over endocannabinoid and fatty acid pathways to support prostate cancer. Chem Biol. 2011;18:846–56.CAS

Nomura DK，Lombardi DP，Chang JW，Niessen S，Ward AM，Long JZ等。单酰基甘油脂肪酶对内源性大麻素和脂肪酸途径发挥双重控制作用，以支持前列腺癌。化学生物学。2011年；18： 846–56.CAS

PubMed

PubMed

PubMed Central

公共医学中心

Google Scholar

谷歌学者

Awad D, Cao PHA, Pulliam TL, Spradlin M, Subramani E, Tellman TV, et al. Adipose triglyceride lipase is a therapeutic target in advanced prostate cancer that promotes metabolic plasticity. Cancer Res. 2024;84:703–24.CAS

Awad D，Cao PHA，Pulliam TL，Spradlin M，Subramani E，Tellman TV等。脂肪甘油三酯脂肪酶是晚期前列腺癌的治疗靶点，可促进代谢可塑性。；84:703–24.CAS

PubMed

PubMed

Google Scholar

谷歌学者

Liu Y. Fatty acid oxidation is a dominant bioenergetic pathway in prostate cancer. Prostate Cancer Prostatic Dis. 2006;9:230–4.CAS

Liu Y.脂肪酸氧化是前列腺癌中主要的生物能量途径。前列腺癌前列腺疾病。；9： 230–4.CAS

PubMed

PubMed

Google Scholar

谷歌学者

Flaig TW, Salzmann-Sullivan M, Su LJ, Zhang Z, Joshi M, Gijón MA, et al. Lipid catabolism inhibition sensitizes prostate cancer cells to antiandrogen blockade. Oncotarget. 2017;8:56051–65.PubMed

Flaig TW，Salzmann-Sullivan M，Su LJ，Zhang Z，Joshi M，Gijón MA等。脂质分解代谢抑制使前列腺癌细胞对抗雄激素阻断敏感。Oncotarget。2017年；8：

PubMed Central

公共医学中心

Google Scholar

谷歌学者

Schlaepfer IR, Rider L, Rodrigues LU, Gijón MA, Pac CT, Romero L, et al. Lipid catabolism via CPT1 as a therapeutic target for prostate cancer. Mol Cancer Ther. 2014;13:2361–71.CAS

Schlaepfer IR，Rider L，Rodrigues LU，Gijón MA，Pac CT，Romero L等。通过CPT1作为前列腺癌治疗靶点的脂质分解代谢。摩尔癌症治疗。2014年；13： 2361-71.CAS

PubMed

PubMed

PubMed Central

公共医学中心

Google Scholar

谷歌学者

Blomme A, Ford CA, Mui E, Patel R, Ntala C, Jamieson LE, et al. 2,4-dienoyl-CoA reductase regulates lipid homeostasis in treatment-resistant prostate cancer. Nat Commun. 2020;11:1–17.

。纳特公社。2020年；11： 1-17岁。

Google Scholar

谷歌学者

Nassar ZD, Mah CY, Dehairs J, Burvenich IJG, Irani S, Centenera MM, et al. Human DECR1 is an androgen-repressed survival factor that regulates PUFA oxidation to protect prostate tumor cells from ferroptosis. Elife. 2020;9:1–34.

Nassar ZD，Mah CY，Dehairs J，Burvenich IJG，Irani S，Centenera MM等。人DECR1是一种雄激素抑制的存活因子，可调节PUFA氧化以保护前列腺肿瘤细胞免受铁浓化。埃利夫。2020年；9： 1-34岁。

Google Scholar

谷歌学者

O’Sullivan SE, Kaczocha M. FABP5 as a novel molecular target in prostate cancer. Drug Discov Today. 2020;25:2056–61.

。今天发现了毒品。2020年；25:2056年至61年。

Google Scholar

谷歌学者

Hillowe A, Gordon C, Wang L, Rizzo RC, Trotman LC, Ojima I, et al. Fatty acid binding protein 5 regulates docetaxel sensitivity in taxane-resistant prostate cancer cells. PLoS One. 2023;18:e0292483.CAS

Hillowe A，Gordon C，Wang L，Rizzo RC，Trotman LC，Ojima I等。脂肪酸结合蛋白5调节紫杉烷耐药前列腺癌细胞对多西紫杉醇的敏感性。PLoS One。2023年；18： e0292483.CAS

PubMed

PubMed

PubMed Central

公共医学中心

Google Scholar

谷歌学者

Carbonetti G, Converso C, Clement T, Wang C, Trotman LC, Ojima I, et al. Docetaxel/cabazitaxel and fatty acid binding protein 5 inhibitors produce synergistic inhibition of prostate cancer growth. Prostate. 2020;80:88–98.CAS

Carbonetti G，Converso C，Clement T，Wang C，Trotman LC，Ojima I等。多西紫杉醇/卡巴他赛和脂肪酸结合蛋白5抑制剂对前列腺癌生长产生协同抑制作用。前列腺。2020年；80:88–98.CAS

PubMed

PubMed

Google Scholar

谷歌学者

M Swamynathan M, Mathew G, Aziz A, Gordon C, Hillowe A, Wang H, et al. FABP5 inhibition against PTEN-mutant therapy resistant prostate cancer. Cancers (Basel). 2023;16:60.PubMed

M Swamynathan M，Mathew G，Aziz A，Gordon C，Hillowe A，Wang H等。FABP5抑制PTEN突变治疗抵抗性前列腺癌。癌症（巴塞尔）。2023年；16： 60.PubMed

Google Scholar

谷歌学者

Watt MJ, Clark AK, Selth LA, Haynes VR, Lister N, Rebello R, et al. Suppressing fatty acid uptake has therapeutic effects in preclinical models of prostate cancer. Sci Transl Med. 2019;11:1–12.Pascual G, Avgustinova A, Mejetta S, Martín M, Castellanos A, Attolini CSO, et al. Targeting metastasis-initiating cells through the fatty acid receptor CD36.

Watt MJ，Clark AK，Selth LA，Haynes VR，Lister N，Rebello R等。抑制脂肪酸摄取在前列腺癌的临床前模型中具有治疗作用。Sci Transl Med。2019；11： 1-12.Pascual G，Avgustinova A，Mejetta S，Martín M，Castellanos A，Attolini CSO等。通过脂肪酸受体CD36靶向转移起始细胞。

Nature. 2017;541:41–45.CAS .

自然。2017年；541:41-45。科学院。

PubMed

PubMed

Google Scholar

谷歌学者

Pascual G, Domínguez D, Elosúa-Bayes M, Beckedorff F, Laudanna C, Bigas C, et al. Dietary palmitic acid promotes a prometastatic memory via Schwann cells. Nature. 2021;599:485–90.CAS

Pascual G，Domínguez D，Elosúa-Bayes M，Beckedorff F，Laudanna C，Bigas C等。膳食棕榈酸通过雪旺氏细胞促进前转移记忆。自然。2021年；599:485–90.CAS

PubMed

PubMed

Google Scholar

谷歌学者

Stopsack KH, Gerke TA, Sinnott JA, Penney KL, Tyekucheva S, Sesso HD, et al. Cholesterol metabolism and prostate cancer lethality. Cancer Res. 2016;76:4785–90.CAS

Stopsack KH，Gerke TA，Sinnott JA，Penney KL，Tyekucheva S，Sesso HD等。胆固醇代谢和前列腺癌致死率。癌症研究2016；76:4785–90.CAS

PubMed

PubMed

PubMed Central

公共医学中心

Google Scholar

谷歌学者

Tibbo AJ, Hartley A, Vasan R, Shaw R, Galbraith L, Mui E, et al. MBTPS2 acts as a regulator of lipogenesis and cholesterol synthesis through SREBP signalling in prostate cancer. Br J Cancer. 2023;128:1991–9.CAS

Tibbo AJ，Hartley A，Vasan R，Shaw R，Galbraith L，Mui E等。MBTPS2通过前列腺癌中的SREBP信号传导充当脂肪生成和胆固醇合成的调节剂。Br J癌症。2023年；128:1991-9.CAS

PubMed

PubMed

PubMed Central

公共医学中心

Google Scholar

谷歌学者

Jiang S, Wang X, Song D, Liu XJ, Gu Y, Xu Z, et al. Cholesterol induces epithelial-to-mesenchymal transition of prostate cancer cells by suppressing degradation of EGFR through APMAP. Cancer Res. 2019;79:3063–75.CAS

蒋S，王X，宋D，刘XJ，顾Y，徐Z，等。胆固醇通过APMAP抑制EGFR的降解，诱导前列腺癌细胞的上皮-间质转化。癌症研究2019；79:3063–75.CAS

PubMed

PubMed

Google Scholar

谷歌学者

Solanki AA, Liauw SL. Role of HMG-CoA reductase inhibitors with curative radiotherapy in men with prostate cancer. Open Access J Urol. 2011;3:95–104.PubMed

。开放存取J Urol。2011年；3： 95-104.PubMed

PubMed Central

公共医学中心

Google Scholar

谷歌学者

Dillard PR, Lin MF, Khan SA. Androgen-independent prostate cancer cells acquire the complete steroidogenic potential of synthesizing testosterone from cholesterol. Mol Cell Endocrinol. 2008;295:115–20.CAS

Dillard PR，Lin MF，Khan SA。雄激素非依赖性前列腺癌细胞具有从胆固醇合成睾酮的完全类固醇生成潜力。摩尔细胞内分泌。2008年；295:115–20.CAS

PubMed

PubMed

PubMed Central

公共医学中心

Google Scholar

谷歌学者

Locke JA, Nelson CC, Adomat HH, Hendy SC, Gleave ME, Guns EST. Steroidogenesis inhibitors alter but do not eliminate androgen synthesis mechanisms during progression to castration-resistance in LNCaP prostate xenografts. J Steroid Biochem Mol Biol. 2009;115:126–36.CAS

洛克JA，纳尔逊CC，阿多马特HH，亨迪SC，格里夫ME，枪炮EST。类固醇生成抑制剂在LNCaP前列腺异种移植物中进展为去势抵抗期间改变但不消除雄激素合成机制。J类固醇生物化学分子生物学。2009年；115:126–36.CAS

PubMed

PubMed

Google Scholar

谷歌学者

Locke JA, Guns ES, Lubik AA, Adomat HH, Hendy SC, Wood CA, et al. Androgen levels increase by intratumoral de novo steroidogenesis during progression of castration-resistant prostate cancer. Cancer Res. 2008;68:6407–15.CAS

Locke JA，Guns ES，Lubik AA，Adomat HH，Hendy SC，Wood CA等。在去势抵抗性前列腺癌的进展过程中，肿瘤内从头类固醇生成会增加雄激素水平。癌症研究2008；68:6407–15.CAS

PubMed

PubMed

Google Scholar

谷歌学者

Raftopulos NL, Washaya TC, Niederprüm A, Egert A, Hakeem-Sanni MF, Varney B, et al. Prostate cancer cell proliferation is influenced by LDL-cholesterol availability and cholesteryl ester turnover. Cancer Metab. 2022;10:1–15.PubMed

Raftopulos NL，Washaya TC，Niederprüm A，Egert A，Hakeem Sanni MF，Varney B等。前列腺癌细胞增殖受LDL胆固醇可用性和胆固醇酯周转率的影响。癌症代谢。2022年；10： 1-15.PubMed

PubMed Central

公共医学中心

Google Scholar

谷歌学者

Murtola TJ, Siltari A. Statins for prostate cancer: when and how much? Clin Cancer Res. 2021;27:4947–9.CAS

Murtola TJ，Siltari A.他汀类药物治疗前列腺癌：何时和多少？Clin Cancer Res.2021；27:4947–9.CAS

PubMed

PubMed

Google Scholar

谷歌学者

Pan T, Lin SC, Lee YC, Yu G, Song JH, Pan J, et al. Statins reduce castration-induced bone marrow adiposity and prostate cancer progression in bone. Oncogene. 2021;40:4592–603.CAS

Pan T，Lin SC，Lee YC，Yu G，Song JH，Pan J等。他汀类药物可减少去势诱导的骨髓肥胖和骨骼中前列腺癌的进展。致癌基因。2021年；40:4592–603.CAS

PubMed

PubMed

PubMed Central

公共医学中心

Google Scholar

谷歌学者

Hoque A, Chen H, Xu XC. Statin induces apoptosis and cell growth arrest in prostate cancer cells. Cancer Epidemiol Biomark Prev. 2008;17:88–94.CAS

霍克A，陈H，徐XC。他汀类药物诱导前列腺癌细胞凋亡和细胞生长停滞。癌症流行病学生物标志物。2008年；17： 88–94.CAS

Google Scholar

谷歌学者

Caro-Maldonado A, Camacho L, Zabala-Letona A, Torrano V, Fernández-Ruiz S, Zamacola-Bascaran K, et al. Low-dose statin treatment increases prostate cancer aggressiveness. Oncotarget. 2017;9:1494–504.PubMed

Caro Maldonado A，Camacho L，Zabala Letona A，Torrano V，Fernández Ruiz S，Zamacola Bascaran K等。低剂量他汀类药物治疗可增加前列腺癌的侵袭性。Oncotarget。2017年；9： 1494-504.PubMed

PubMed Central

公共医学中心

Google Scholar

谷歌学者

Shangguan X, Ma Z, Yu M, Ding J, Xue W, Qi J. Squalene epoxidase metabolic dependency is a targetable vulnerability in castration-resistant prostate cancer. Cancer Res. 2022;82:3032–44.CAS

Shangguan X，Ma Z，Yu M，Ding J，Xue W，Qi J.角鲨烯环氧化酶代谢依赖性是去势抵抗性前列腺癌的可靶向脆弱性。癌症研究2022；82:3032-44.CAS

PubMed

PubMed

Google Scholar

谷歌学者

Kalogirou C, Linxweiler J, Schmucker P, Snaebjornsson MT, Schmitz W, Wach S, et al. MiR-205-driven downregulation of cholesterol biosynthesis through SQLE-inhibition identifies therapeutic vulnerability in aggressive prostate cancer. Nat Commun. 2021;12:5066.CAS

Kalogirou C，Linxweiler J，Schmucker P，Snaebjornsson MT，Schmitz W，Wach S等。通过SQLE抑制MiR-205驱动的胆固醇生物合成下调确定了侵袭性前列腺癌的治疗脆弱性。纳特公社。2021年；12：

PubMed

PubMed

PubMed Central

公共医学中心

Google Scholar

谷歌学者

El-Kenawi A, Dominguez-Viqueira W, Liu M, Awasthi S, Abraham-Miranda J, Keske A, et al. Macrophage-derived cholesterol contributes to therapeutic resistance in prostate cancer. Cancer Res. 2021;81:5477–90.CAS

El Kenawi A，Dominguez-Viqueira W，Liu M，Awasthi S，Abraham Miranda J，Keske A等。巨噬细胞衍生的胆固醇有助于前列腺癌的治疗抵抗。癌症研究2021；81:5477–90.CAS

PubMed

PubMed

PubMed Central

公共医学中心

Google Scholar

谷歌学者

Ducker GS, Rabinowitz JD. One-carbon metabolism in health and disease. Cell Metab. 2017;25:27–42.CAS

Ducker GS，Rabinowitz JD。健康和疾病中的单碳代谢。细胞代谢。2017年；25:27–42.CAS

PubMed

PubMed

Google Scholar

谷歌学者

Islam A, Shaukat Z, Hussain R, Gregory SL. One-carbon and polyamine metabolism as cancer therapy targets. Biomolecules. 2022;12:1902.CAS

Islam A，Shaukat Z，Hussain R，Gregory SL.单碳和多胺代谢作为癌症治疗靶点。生物分子。2022年；12： 1902年

PubMed

PubMed

PubMed Central

公共医学中心

Google Scholar

谷歌学者

Newman AC, Maddocks ODK. One-carbon metabolism in cancer. Br J Cancer. 2017;116:1499–504.CAS

纽曼AC，马多克斯ODK。癌症中的单碳代谢。Br J癌症。2017年；116:1499-504.CAS

PubMed

PubMed

PubMed Central

公共医学中心

Google Scholar

谷歌学者

Yang M, Vousden KH. Serine and one-carbon metabolism in cancer. Nat Rev Cancer. 2016;16:650–62.CAS

Yang M，Vousden KH。癌症中的丝氨酸和一碳代谢。。；16： 650–62.CAS

PubMed

PubMed

Google Scholar

谷歌学者

Corbin JM, Ruiz-Echevarría MJ. One-carbon metabolism in prostate cancer: the role of androgen signaling. Int J Mol Sci. 2016;17:1208.PubMed

科尔宾JM，鲁伊斯·埃切瓦里亚MJ。前列腺癌中的单碳代谢：雄激素信号传导的作用。国际分子科学杂志。；17： 1208.PubMed

PubMed Central

公共医学中心

Google Scholar

谷歌学者

Green T, Chen X, Ryan S, Asch AS, Ruiz-Echevarría MJ. TMEFF2 and SARDH cooperate to modulate one-carbon metabolism and invasion of prostate cancer cells. Prostate. 2013;73:1561–75.CAS

Green T，Chen X，Ryan S，Asch AS，Ruiz Echevarría MJ。TMEFF2和SARDH合作调节单碳代谢和前列腺癌细胞的侵袭。前列腺。2013年；73:1561-75.CAS

PubMed

PubMed

Google Scholar

谷歌学者

Song YH, Shiota M, Kuroiwa K, Naito S, Oda Y. The important role of glycine N-methyltransferase in the carcinogenesis and progression of prostate cancer. Mod Pathol. 2011;24:1272–80.CAS

Song YH，Shiota M，Kuroiwa K，Naito S，Oda Y.甘氨酸N-甲基转移酶在前列腺癌发生和发展中的重要作用。Mod病理学。2011年；24:1272–80.CAS

PubMed

PubMed

Google Scholar

谷歌学者

Khan AP, Rajendiran TM, Ateeq B, Asangani IA, Athanikar JN, Yocum AK, et al. The role of sarcosine metabolism in prostate cancer progression. Neoplasia. 2013;15:491–501.CAS

Khan AP，Rajendiran TM，Ateeq B，Asangani IA，Athanikar JN，Yocum AK等。肌氨酸代谢在前列腺癌进展中的作用。瘤形成。2013年；15： 491–501.CAS

PubMed

PubMed

PubMed Central

公共医学中心

Google Scholar

谷歌学者

Jentzmik F, Stephan C, Lein M, Miller K, Kamlage B, Bethan B, et al. Sarcosine in prostate cancer tissue is not a differential metabolite for prostate cancer aggressiveness and biochemical progression. J Urol. 2011;185:706–11.CAS

Jentzmik F，Stephan C，Lein M，Miller K，Kamlage B，Bethan B等。前列腺癌组织中的肌氨酸不是前列腺癌侵袭性和生化进展的差异代谢物。J乌拉尔。2011年；185:706-11.CAS

PubMed

PubMed

Google Scholar

谷歌学者

Sreekumar A, Poisson LM, Rajendiran TM, Khan AP, Cao Q, Yu J, et al. Metabolomic profiles delineate potential role for sarcosine in prostate cancer progression. Nature. 2009;457:910–4.CAS

Sreekumar A，Poisson LM，Rajendiran TM，Khan AP，Cao Q，Yu J等。代谢组学特征描述了肌氨酸在前列腺癌进展中的潜在作用。自然。2009年；457:910–4.CAS

PubMed

PubMed

PubMed Central

公共医学中心

Google Scholar

谷歌学者

Luka Z, Mudd SH, Wagner C. Glycine N-methyltransferase and regulation of S-adenosylmethionine levels. J Biol Chem. 2009;284:22507–11.CAS

Luka Z，Mudd SH，Wagner C.甘氨酸N-甲基转移酶和S-腺苷甲硫氨酸水平的调节。生物化学杂志。2009年；284:22507–11.CAS

PubMed

PubMed

PubMed Central

公共医学中心

Google Scholar

谷歌学者

Ottaviani S, Brooke GN, O’Hanlon-Brown C, Waxman J, Ali S, Buluwela L. Characterisation of the androgen regulation of glycine N-methyltransferase in prostate cancer cells. J Mol Endocrinol. 2013;51:301–12.CAS

Ottaviani S，Brooke GN，O'Hanlon-Brown C，Waxman J，Ali S，Buluwela L.前列腺癌细胞中甘氨酸N-甲基转移酶的雄激素调节的表征。J摩尔内分泌。2013年；51:301–12.CAS

PubMed

PubMed

PubMed Central

公共医学中心

Google Scholar

谷歌学者

Mulholland DJ, Tran LM, Li Y, Cai H, Morim A, Wang S, et al. Cell autonomous role of PTEN in regulating castration-resistant prostate cancer growth. Cancer Cell. 2011;19:792–804.CAS

Mulholland DJ，Tran LM，Li Y，Cai H，Morim A，Wang S等。PTEN在调节去势抵抗性前列腺癌生长中的细胞自主作用。癌细胞。2011年；19： 792–804.CAS

PubMed

PubMed

PubMed Central

公共医学中心

Google Scholar

谷歌学者

Carver BS, Chapinski C, Wongvipat J, Hieronymus H, Chen Y, Chandarlapaty S, et al. Reciprocal feedback regulation of PI3K and androgen receptor signaling in PTEN-deficient prostate cancer. Cancer Cell. 2011;19:575–86.CAS

Carver BS，Chapinski C，Wongvipat J，Hieronymus H，Chen Y，Chandarlapaty S等。PTEN缺陷型前列腺癌中PI3K和雄激素受体信号传导的相互反馈调节。癌细胞。2011年；19： 575–86.CAS

PubMed

PubMed

PubMed Central

公共医学中心

Google Scholar

谷歌学者

Zabala-Letona A, Arruabarrena-Aristorena A, Fernandez-Ruiz S, Viera C, Carlevaris O, Ercilla A, et al. PI3K-regulated Glycine N-methyltransferase is required for the development of prostate cancer. Oncogenesis. 2022;11:10.Obata F, Miura M. Enhancing S-adenosyl-methionine catabolism extends Drosophila lifespan.

Zabala Letona A，Arruabarena Aristorena A，Fernandez-Ruiz S，Viera C，Carlevaris O，Ercilla A等。PI3K调节的甘氨酸N-甲基转移酶是前列腺癌发展所必需的。肿瘤发生。2022年；11： Obata F，Miura M.增强S-腺苷甲硫氨酸分解代谢可延长果蝇的寿命。

Nat Commun. 2015;6:1–9..

普通NAT。2015年；6:1-9。

Google Scholar

谷歌学者

Reina-Campos M, Linares JF, Duran A, Cordes T, L’Hermitte A, Badur MG, et al. Increased serine and one-carbon pathway metabolism by PKCλ/ι deficiency promotes neuroendocrine prostate cancer. Cancer Cell. 2019;35:385–400.e9.CAS

Reina Campos M，Linares JF，Duran A，Cordes T，L'Hermitte A，Badur MG等。PKCλ/ι缺乏引起的丝氨酸和单碳途径代谢增加会促进神经内分泌前列腺癌。癌细胞。2019年；35:385–400.e9.CAS

PubMed

PubMed

PubMed Central

公共医学中心

Google Scholar

谷歌学者

Zhang HF, Klein Geltink RI, Parker SJ, Sorensen PH. Transsulfuration, minor player or crucial for cysteine homeostasis in cancer. Trends Cell Biol. 2022;32:800–14.PubMed

Zhang HF，Klein Geltink RI，Parker SJ，Sorensen PH。转硫，次要参与者或对癌症中半胱氨酸稳态至关重要。趋势细胞生物学。2022年；32:800–14.PubMed

PubMed Central

公共医学中心

Google Scholar

谷歌学者

Prudova A, Albin M, Bauman Z, Lin A, Vitvitsky V, Banerjee R. Testosterone regulation of homocysteine metabolism modulates redox status in human prostate cancer cells. Antioxid Redox Signal. 2007;9:1875–81.CAS

Prudova A，Albin M，Bauman Z，Lin A，Vitvitsky V，Banerjee R.同型半胱氨酸代谢的睾酮调节调节人前列腺癌细胞中的氧化还原状态。抗氧化氧化还原信号。2007年；9： 1875-81年

PubMed

PubMed

Google Scholar

谷歌学者

Guo H, Gai JW, Wang Y, Jin HF, Du JB, Jin J. Characterization of hydrogen sulfide and its synthases, cystathionine β-synthase and cystathionine γ-lyase, in human prostatic tissue and cells. Urology. 2012;79:483.e1–483.e5.PubMed

Guo H，Gai JW，Wang Y，Jin HF，Du JB，Jin J.人前列腺组织和细胞中硫化氢及其合酶，胱硫醚β-合酶和胱硫醚γ-裂解酶的表征。泌尿外科。2012年；79:483。e1–483.e5.PubMed

Google Scholar

谷歌学者

Zhang W, Braun A, Bauman Z, Olteanu H, Madzelan P, Banerjee R. Expression profiling of homocysteine junction enzymes in the NCI60 panel of human cancer cell lines. Cancer Res. 2005;65:1554–60.CAS

Zhang W，Braun A，Bauman Z，Olteanu H，Madzelan P，Banerjee R.人类癌细胞系NCI60组中同型半胱氨酸连接酶的表达谱。癌症研究2005；65:1554–60.CAS

PubMed

PubMed

Google Scholar

谷歌学者

Stabler S, Koyama T, Zhao Z, Martinez-Ferrer M, Allen RH, Luka Z et al. Serum methionine metabolites are risk factors for metastatic prostate cancer progression. PLoS One 2011;6:8.Saha A, Zhao S, Kindall A, Wilder C, Friedman CA, Clark R et al. Cysteine depletion sensitizes prostate cancer cells to agents that enhance DNA damage and to immune checkpoint inhibition.

。PLoS One 2011；6： Saha A，Zhao S，Kindall A，Wilder C，Friedman CA，Clark R等人。半胱氨酸耗竭使前列腺癌细胞对增强DNA损伤和免疫检查点抑制的药物敏感。

J Exp Clin Cancer Res. 2023;42:119.Pegg AE. Functions of polyamines in mammals. J Biol Chem. 2016;291:14904–12.CAS .

J Exp Clin Cancer Res.2023；42:119.Pegg AE。多胺在哺乳动物中的功能。生物化学杂志。；291:14904-12。CAS。

PubMed

PubMed

PubMed Central

公共医学中心

Google Scholar

谷歌学者

Nowotarski SL, Woster PM, Casero RA Jr. Polyamines and cancer: implications for chemoprevention and chemotherapy. Expert Rev Mol Med. 2014;15:1–28.

Nowotarski SL，Woster PM，Casero RA Jr。多胺与癌症：对化学预防和化疗的影响。专家Rev Mol Med。2014；15： 1-28岁。

Google Scholar

谷歌学者

Jänne OA, Crozat A, Palvimo J, Eisenberg LM. Androgen-regulation of ornithine decarboxylase and S-adenosylmethionine decarboxylase genes. J Steroid Biochem Mol Biol. 1991;40:307–15.PubMed

Jänne OA，Crozat A，Palvimo J，Eisenberg LM。雄激素调节鸟氨酸脱羧酶和S-腺苷甲硫氨酸脱羧酶基因。J类固醇生物化学分子生物学。1991年；40:307–15.PubMed

Google Scholar

谷歌学者

Fjösne HE, Strand H, Sunde A. Dose-dependent induction of ornithine decarboxylase and S-adenosyl-methionine decarboxylase activity by testosterone in the accessory sex organs of male rats. Prostate. 1992;21:239–45.PubMed

Fjösne HE，Strand H，Sunde A.雄性大鼠辅助性器官中睾酮对鸟氨酸脱羧酶和S-腺苷甲硫氨酸脱羧酶活性的剂量依赖性诱导。前列腺。1992年；21:239–45.PubMed

Google Scholar

谷歌学者

Cohen RJ, Fujiwara K, Holland JW, McNeal JE. Polyamines in prostatic epithelial cells and adenocarcinoma; the effects of androgen blockade. Prostate. 2001;49:278–84.CAS

Cohen RJ，Fujiwara K，Holland JW，McNeal JE。前列腺上皮细胞和腺癌中的多胺；雄激素阻断的作用。前列腺。2001年；49:278–84.CAS

PubMed

PubMed

Google Scholar

谷歌学者

Bello-Fernandez C, Packham G, Cleveland JL. The ornithine decarboxylase gene is a transcriptional target of c-Myc. Proc Natl Acad Sci USA. 1993;90:7804–8.CAS

Bello Fernandez C，Packham G，克利夫兰JL。鸟氨酸脱羧酶基因是c-Myc的转录靶标。美国国家科学院院刊1993；90:7804–8.CAS

PubMed

PubMed

PubMed Central

公共医学中心

Google Scholar

谷歌学者

Kaminski L, Torrino S, Dufies M, Djabari Z, Haider R, Roustan FR, et al. PGC1α inhibits polyamine synthesis to suppress prostate cancer aggressiveness. Cancer Res. 2019;79:3268–80.CAS

Kaminski L，Torrino S，Dufies M，Djabari Z，Haider R，Roustan FR等。PGC1α抑制多胺合成以抑制前列腺癌的侵袭性。癌症研究2019；

PubMed

PubMed

PubMed Central

公共医学中心

Google Scholar

谷歌学者

Torrano V, Valcarcel-Jimenez L, Cortazar AR, Liu X, Urosevic J, Castillo-Martin M, et al. The metabolic co-regulator PGC1α suppresses prostate cancer metastasis. Nat Cell Biol. 2016;18:645–56.CAS

Torrano V，Valcarcel Jimenez L，Cortazar AR，Liu X，Urosevic J，Castillo Martin M等。代谢协同调节剂PGC1α抑制前列腺癌转移。Nat细胞生物学。；18： 645–56.CAS

PubMed

PubMed

PubMed Central

公共医学中心

Google Scholar

谷歌学者

Valcarcel-Jimenez L, Macchia A, Crosas-Molist E, Schaub-Clerigue A, Camacho L, Martín-Martín N, et al. PGC1α suppresses prostate cancer cell invasion through ERRα transcriptional control. Cancer Res. 2019;79:6153–65.CAS

Valcarcel-Jimenez L，Macchia A，Crosas-Molist E，Schaub Clerigue A，Camacho L，Martín-Martín等。PGC1α通过ERRα转录控制抑制前列腺癌细胞的侵袭。癌症研究2019；79:6153–65.CAS

PubMed

PubMed

Google Scholar

谷歌学者

Zabala-Letona A, Arruabarrena-Aristorena A, Martín-Martín N, Fernandez-Ruiz S, Sutherland JD, Clasquin M, et al. MTORC1-dependent AMD1 regulation sustains polyamine metabolism in prostate cancer. Nature. 2017;547:109–13.CAS

Zabala Letona A，Arruabarena Aristorena A，Martín-Martín n，Fernandez-Ruiz S，Sutherland JD，Clasquin M等。依赖MTORC1的AMD1调节维持前列腺癌中的多胺代谢。自然。2017年；547:109–13.CAS

PubMed

PubMed

PubMed Central

公共医学中心

Google Scholar

谷歌学者

Monelli E, Villacampa P, Zabala-Letona A, Martinez-Romero A, Llena J, Beiroa D, et al. Angiocrine polyamine production regulates adiposity. Nat Metab. 2022;4:327–43.CAS

Monelli E，Villacampa P，Zabala Letona A，Martinez Romero A，Llena J，Beiroa D等。血管分泌多胺的产生调节脂肪。Nat Metab。2022;4:327–43.CAS编号4:327–43.2CAS编号4:327-43。

PubMed

PubMed

Google Scholar

谷歌学者

de Visser KE, Joyce JA. The evolving tumor microenvironment: from cancer initiation to metastatic outgrowth. Cancer Cell. 2023;41:374–403.PubMed

。不断发展的肿瘤微环境：从癌症起始到转移性生长。癌细胞。2023年；41:374–403.PubMed

Google Scholar

谷歌学者

Qin Y, Lu F, Lyu K, Chang AE, Li Q. Emerging concepts regarding pro- and anti tumor properties of B cells in tumor immunity. Front Immunol. 2022;13:881427.Chen S, Zhu G, Yang Y, Wang F, Xiao YT, Zhang N, et al. Single-cell analysis reveals transcriptomic remodellings in distinct cell types that contribute to human prostate cancer progression.

Qin Y，Lu F，Lyu K，Chang AE，Li Q.关于B细胞在肿瘤免疫中的促肿瘤和抗肿瘤特性的新兴概念。前免疫。2022年；13： 单细胞分析揭示了不同细胞类型的转录组重塑，这些细胞类型有助于人类前列腺癌的进展。

Nat Cell Biol. 2021;23:87–98.CAS .

Nat细胞生物学。2021;23:87–98.CAS[联合王国]。

PubMed

PubMed

Google Scholar

谷歌学者

Wong HY, Sheng Q, Hesterberg AB, Croessmann S, Rios BL, Giri K, et al. Single cell analysis of cribriform prostate cancer reveals cell intrinsic and tumor microenvironmental pathways of aggressive disease. Nat Commun. 2022;13:6036.Lopez-Bujanda ZA, Haffner MC, Chaimowitz MG, Chowdhury N, Venturini NJ, Patel RA, et al.

Wong HY，Sheng Q，Hesterberg AB，Croessmann S，Rios BL，Giri K等。筛状前列腺癌的单细胞分析揭示了侵袭性疾病的细胞内在和肿瘤微环境途径。纳特公社。2022年；13： 6036.Lopez-Bujanda ZA，Haffner MC，Chaimowitz MG，Chowdhury N，Venturini NJ，Patel RA等。

Castration-mediated IL-8 promotes myeloid infiltration and prostate cancer progression. Nat Cancer. 2021;2:803–18.CAS .

去势介导的IL-8促进骨髓浸润和前列腺癌进展。Nat癌症。2021年；2： 803-18年。

PubMed

PubMed

PubMed Central

公共医学中心

Google Scholar

谷歌学者

Chang C-H, Qiu J, O’Sullivan D, Buck MD, Noguchi T, Curtis JD, et al. Metabolic competition in the tumor microenvironment is a driver of cancer progression. Cell. 2015;162:1229–41.CAS

Chang C-H，Qiu J，O'Sullivan D，Buck MD，Noguchi T，Curtis JD等。肿瘤微环境中的代谢竞争是癌症进展的驱动因素。细胞。2015年；162:1229-41.CAS

PubMed

PubMed

PubMed Central

公共医学中心

Google Scholar

谷歌学者

Beckermann KE, Dudzinski SO, Rathmell JC. Dysfunctional T cell metabolism in the tumor microenvironment. Cytokine Growth Factor Rev. 2017;35:7–14.CAS

贝克曼·科（Beckermann KE），杜津斯基·苏（Dudzinski SO），拉斯梅尔（Rathmell JC）。肿瘤微环境中功能失调的T细胞代谢。细胞因子生长因子Rev.2017；35:7–14.CAS

PubMed

PubMed

PubMed Central

公共医学中心

Google Scholar

谷歌学者

Estrella V, Chen T, Lloyd M, Wojtkowiak J, Cornnell HH, Ibrahim-Hashim A, et al. Acidity generated by the tumor microenvironment drives local invasion. Cancer Res. 2013;73:1524–35.CAS

Estrella V，Chen T，Lloyd M，Wojtkowiak J，Cornnell HH，Ibrahim Hashim A等。肿瘤微环境产生的酸度驱动局部侵袭。癌症研究2013；73:1524–35.CAS

PubMed

PubMed

PubMed Central

公共医学中心

Google Scholar

谷歌学者

Liberti MV, Locasale JW. The Warburg effect: how does it benefit cancer cells? Trends Biochem Sci. 2016;41:211–8.CAS

Liberti MV，Locasale JW。Warburg效应：它如何使癌细胞受益？。；41:211–8.CAS

PubMed

PubMed

PubMed Central

公共医学中心

Google Scholar

谷歌学者

Niu D, Wu Y, Lei Z, Zhang M, Xie Z, Tang S. Lactic acid, a driver of tumor-stroma interactions. Int Immunopharmacol. 2022;106:108597.CAS

牛D，吴Y，雷Z，张M，谢Z，唐S。乳酸，肿瘤-基质相互作用的驱动因素。国际免疫药理学。2022年；106:108597.CAS

PubMed

PubMed

Google Scholar

谷歌学者

Fischer K, Hoffmann P, Voelkl S, Meidenbauer N, Ammer J, Edinger M, et al. Inhibitory effect of tumor cell-derived lactic acid on human T cells. Blood. 2007;109:3812–9.CAS

Fischer K，Hoffmann P，Voelkl S，Meidenbauer N，Ammer J，Edinger M等。肿瘤细胞衍生乳酸对人T细胞的抑制作用。血。2007年；109:3812-9.CAS

PubMed

PubMed

Google Scholar

谷歌学者

Inamdar S, Suresh AP, Mangal JL, Ng ND, Sundem A, Wu C, et al. Rescue of dendritic cells from glycolysis inhibition improves cancer immunotherapy in mice. Nat Commun. 2023;14:5333.CAS

Inamdar S，Suresh AP，Mangal JL，Ng ND，Sundem A，Wu C等。从糖酵解抑制中拯救树突状细胞可改善小鼠的癌症免疫疗法。纳特公社。2023年；14： 5333.CAS

PubMed

PubMed

PubMed Central

公共医学中心

Google Scholar

谷歌学者

Chang C-H, Curtis JD, Maggi LBJ, Faubert B, Villarino AV, O’Sullivan D, et al. Posttranscriptional control of T cell effector function by aerobic glycolysis. Cell. 2013;153:1239–51.CAS

Chang C-H，Curtis JD，Maggi LBJ，Faubert B，Villarino AV，O'Sullivan D等。通过有氧糖酵解对T细胞效应子功能的转录后控制。细胞。2013年；153:1239-51.CAS

PubMed

PubMed

PubMed Central

公共医学中心

Google Scholar

谷歌学者

Jacobs SR, Herman CE, Maciver NJ, Wofford JA, Wieman HL, Hammen JJ, et al. Glucose uptake is limiting in T cell activation and requires CD28-mediated Akt-dependent and independent pathways. J Immunol. 2008;180:4476–86.CAS

Jacobs SR，Herman CE，Maciver NJ，Wofford JA，Wieman HL，Hammen JJ等。葡萄糖摄取在T细胞活化中受到限制，需要CD28介导的Akt依赖性和独立途径。免疫杂志。2008年；180:4476–86.CAS

PubMed

PubMed

Google Scholar

谷歌学者

Notarangelo G, Spinelli JB, Perez EM, Baker GJ, Kurmi K, Elia I, et al. Oncometabolite d-2HG alters T cell metabolism to impair CD8( + ) T cell function. Science. 2022;377:1519–29.CAS

Notarangelo G，Spinelli JB，Perez EM，Baker GJ，Kurmi K，Elia I等。Oncometabolicate d-2HG改变T细胞代谢以损害CD8（+）T细胞功能。科学。2022年；377:1519-29.CAS

PubMed

PubMed

PubMed Central

公共医学中心

Google Scholar

谷歌学者

Lim SA, Wei J, Nguyen TLM, Shi H, Su W, Palacios G, et al. Lipid signalling enforces functional specialization of Treg cells in tumours. Nature. 2021;591:306–11.CAS

Lim SA，Wei J，Nguyen TLM，Shi H，Su W，Palacios G等。脂质信号传导增强了肿瘤中Treg细胞的功能特化。自然。2021年；591:306-11.CAS

PubMed

PubMed

PubMed Central

公共医学中心

Google Scholar

谷歌学者

Field CS, Baixauli F, Kyle RL, Puleston DJ, Cameron AM, Sanin DE, et al. Mitochondrial integrity regulated by lipid metabolism is a cell-intrinsic checkpoint for treg suppressive function. Cell Metab. 2020;31:422–37.e5.CAS

Field CS，Baixauli F，Kyle RL，Puleston DJ，Cameron AM，Sanin DE等。脂质代谢调节的线粒体完整性是treg抑制功能的细胞内在检查点。细胞代谢。2020年；31:422–37.e5.CAS

PubMed

PubMed

PubMed Central

公共医学中心

Google Scholar

谷歌学者

Yang P, Qin H, Li Y, Xiao A, Zheng E, Zeng H, et al. CD36-mediated metabolic crosstalk between tumor cells and macrophages affects liver metastasis. Nat Commun. 2022;13:5782.CAS

Yang P，Qin H，Li Y，Xiao A，Zheng E，Zeng H，et al。CD36介导的肿瘤细胞和巨噬细胞之间的代谢串扰影响肝转移。纳特公社。2022年；13： 5782.CAS

PubMed

PubMed

PubMed Central

公共医学中心

Google Scholar

谷歌学者

Nava Lauson CB, Tiberti S, Corsetto PA, Conte F, Tyagi P, Machwirth M, et al. Linoleic acid potentiates CD8 + T cell metabolic fitness and antitumor immunity. Cell Metab. 2023;35:633–50.e9.CAS

Nava Lauson CB，Tiberti S，Corsetto PA，Conte F，Tyagi P，Machwirth M等。亚油酸增强CD8+T细胞代谢适应性和抗肿瘤免疫力。细胞代谢。2023年；35:633–50.e9.CAS

PubMed

PubMed

Google Scholar

谷歌学者

Rowe JH, Elia I, Shahid O, Gaudiano EF, Sifnugel NE, Johnson S, et al. Formate supplementation enhances antitumor CD8 + T-cell fitness and efficacy of PD-1 blockade. Cancer Discov. 2023;13:2566–83.CAS

Rowe JH，Elia I，Shahid O，Gaudiano EF，Sifnugel NE，Johnson S等。甲酸盐补充剂增强抗肿瘤CD8+T细胞适应性和PD-1阻断的功效。癌症发现。2023年；13： 2566–83.CAS

PubMed

PubMed

PubMed Central

公共医学中心

Google Scholar

谷歌学者

Cheng H, Qiu Y, Xu Y, Chen L, Ma K, Tao M, et al. Extracellular acidosis restricts one-carbon metabolism and preserves T cell stemness. Nat Metab. 2023;5:314–30.CAS

Cheng H，Qiu Y，Xu Y，Chen L，Ma K，Tao M等。细胞外酸中毒限制单碳代谢并保持T细胞干性。自然代谢。2023年；5：

PubMed

PubMed

PubMed Central

公共医学中心

Google Scholar

谷歌学者

Kurniawan H, Franchina DG, Guerra L, Bonetti L, Baguet LS, Grusdat M, et al. Glutathione restricts serine metabolism to preserve regulatory T cell function. Cell Metab. 2020;31:920–36.e7.CAS

Kurniawan H，Franchina DG，Guerra L，Bonetti L，Baguet LS，Grusdat M等。谷胱甘肽限制丝氨酸代谢以保持调节性T细胞功能。细胞代谢。2020年；31:920–36.e7.CAS

PubMed

PubMed

PubMed Central

公共医学中心

Google Scholar

谷歌学者

Valera PS, Plou J, García I, Astobiza I, Viera C, Aransay AM, et al. SERS analysis of cancer cell-secreted purines reveals a unique paracrine crosstalk in MTAP-deficient tumors. Proc Natl Acad Sci USA. 2023;120:52.Terry AR, Nogueira V, Rho H, Ramakrishnan G, Li J, Kang S, et al. CD36 maintains lipid homeostasis via selective uptake of monounsaturated fatty acids during matrix detachment and tumor progression.

Valera PS，Plou J，García I，Astobiza I，Viera C，Aransay AM等。癌细胞分泌嘌呤的SERS分析揭示了MTAP缺陷型肿瘤中独特的旁分泌串扰。美国国家科学院院刊2023；120:52.Terry AR，Nogueira V，Rho H，Ramakrishnan G，Li J，Kang S等。CD36通过在基质分离和肿瘤进展过程中选择性摄取单不饱和脂肪酸来维持脂质稳态。

Cell Metab. 2023;35:2060–2076.e9.CAS .

细胞代谢。2023年；35:2060年至2076年。

PubMed

PubMed

Google Scholar

谷歌学者

Kalaany NY, Sabatini DM. Tumours with PI3K activation are resistant to dietary restriction. Nature. 2009;458:725–31.CAS

Kalaany NY，Sabatini DM。具有PI3K激活的肿瘤对饮食限制具有抗性。自然。2009年；458:725–31.CAS

PubMed

PubMed

PubMed Central

公共医学中心

Google Scholar

谷歌学者

Lien EC, Westermark AM, Zhang Y, Yuan C, Li Z, Lau AN, et al. Low glycaemic diets alter lipid metabolism to influence tumour growth. Nature. 2021;599:302–7.CAS

Lien EC，Westermark AM，Zhang Y，Yuan C，Li Z，Lau AN等。低血糖饮食改变脂质代谢以影响肿瘤生长。自然。2021年；599:302–7.CAS

PubMed

PubMed

PubMed Central

公共医学中心

Google Scholar

谷歌学者

Vidal AC, Freedland SJ. Obesity and prostate cancer: a focused update on active surveillance, race, and molecular subtyping. Eur Urol. 2017;72:78.PubMed

Vidal AC，Freedland SJ。肥胖和前列腺癌：关于主动监测，种族和分子亚型的重点更新。Eur Urol公司。2017年；72:78.PubMed

Google Scholar

谷歌学者

Cantarutti A, Bonn SE, Adami HO, Grönberg H, Bellocco R, Bälter K. Body mass index and mortality in men with prostate cancer. Prostate. 2015;75:1129–36.PubMed

Cantarutti A，Bonn SE，Adami HO，Grönberg H，Bellocco R，Bälter K.前列腺癌男性的体重指数和死亡率。前列腺。2015年；75:1129–36.PubMed

Google Scholar

谷歌学者

Zhong S, Yan X, Wu Y, Zhang X, Chen L, Tang J, et al. Body mass index and mortality in prostate cancer patients: a dose-response meta-analysis. Prostate Cancer Prostatic Dis. 2016;19:122–31.CAS

钟S，严X，吴Y，张X，陈L，唐J，等。前列腺癌患者的体重指数和死亡率：剂量反应荟萃分析。前列腺癌前列腺疾病。；19： 122–31.CAS

PubMed

PubMed

Google Scholar

谷歌学者

Liu J, Ramakrishnan SK, Khuder SS, Kaw MK, Muturi HT, Lester SG, et al. High-calorie diet exacerbates prostate neoplasia in mice with haploinsufficiency of Pten tumor suppressor gene. Mol Metab. 2015;4:186–98.CAS

Liu J，Ramakrishnan SK，Khuder SS，Kaw MK，Muturi HT，Lester SG等。高热量饮食会加剧Pten肿瘤抑制基因单倍剂量不足的小鼠的前列腺肿瘤。摩尔代谢。2015年；4： 186–98.CAS

PubMed

PubMed

PubMed Central

公共医学中心

Google Scholar

谷歌学者

Wang H, Yan W, Sun Y, Yang CS. High-fat diet-induced hyperinsulinemia promotes the development of prostate adenocarcinoma in prostate-specific Pten−/− mice. Carcinogenesis. 2022;43:504–16.CAS

王浩，严文，孙毅，杨CS。高脂饮食诱导的高胰岛素血症促进前列腺特异性Pten-/-小鼠前列腺腺癌的发展。致癌作用。2022年；43:504–16.CAS

PubMed

PubMed

Google Scholar

谷歌学者

Labbé DP, Uetani N, Vinette V, Lessard L, Aubry I, Migon E, et al. PTP1B deficiency enables the ability of a high-fat diet to drive the invasive character of PTEN-deficient prostate cancers. Cancer Res. 2016;76:3130–5.PubMed

LabbéDP，Uetani N，Vinette V，Lessard L，Aubry I，Migon E等。PTP1B缺乏症使高脂饮食能够驱动PTEN缺陷型前列腺癌的侵袭性。癌症研究2016；76:3130–5.PubMed

PubMed Central

公共医学中心

Google Scholar

谷歌学者

Hayashi T, Fujita K, Nojima S, Hayashi Y, Nakano K, Ishizuya Y, et al. High-fat diet-induced inflammation accelerates prostate cancer growth via IL6 signaling. Clin Cancer Res. 2018;24:4309–18.CAS

Hayashi T，Fujita K，Nojima S，Hayashi Y，Nakano K，Ishizuya Y等。高脂饮食诱导的炎症通过IL6信号传导加速前列腺癌的生长。；24:4309–18.CAS

PubMed

PubMed

Google Scholar

谷歌学者

Chen M, Zhang J, Sampieri K, Clohessy JG, Mendez L, Gonzalez-Billalabeitia E, et al. An aberrant SREBP-dependent lipogenic program promotes metastatic prostate cancer. Nat Genet. 2018;50:206.CAS

Chen M，Zhang J，Sampieri K，Clohessy JG，Mendez L，Gonzalez-Billalabeitia E等。异常的SREBP依赖性脂肪生成程序促进转移性前列腺癌。纳特·吉内特。2018年；

PubMed

PubMed

PubMed Central

公共医学中心

Google Scholar

谷歌学者

Carreño DV, Corro NBNB, Cerda-Infante JF, Echeverría CE, Asencio-Barría CA, Torres-Estay VAVA, et al. Dietary fructose promotes prostate cancer growth. Cancer Res. 2021;81:2824–32.PubMed

Carrenio DV、Corro NBNB、Cerda-Infante JF、Echeverría CE、Asencio-Barria Ca、Torres-Estay Vava等。饮食果糖促进前列腺癌的生长。癌症研究。2021年；81:2824-32.pubmed

Google Scholar

谷歌学者

Download referencesAcknowledgementsWe are grateful to the Carracedo lab for valuable input, and to Kathrin Keim for the help with English editing. A. Carracedo is funded by the Basque Department of Industry, Tourism and Trade (Elkartek), the BBVA foundation (Becas Leonardo), the MICINN (PID2022-141553OB-I0 (FEDER/EU); La Caixa Foundation (ID 100010434), under the agreement LCF/PR/HR17, Fundación Cris Contra el Cáncer (PR_EX_2021-22), Severo Ochoa Excellence Accreditation CEX2021-001136-S), 2023 AstraZeneca Award for Young scientists in oncology, European Training Networks Project (H2020-MSCA-ITN-308 2016 721532), Vencer el Cáncer Foundation, iDIFFER network of Excellence (RED2022-134792-T), Asociación Española Contra el Cáncer (GCTRA18006CARR) and the European Research Council (Consolidator Grant 819242).

下载参考文献致谢我们感谢Carracedo实验室的宝贵投入，感谢Kathrin Keim对英语编辑的帮助。A、 卡拉塞多由巴斯克工业、旅游和贸易部（Elkartek）、BBVA基金会（Becas Leonardo）、MICINN（PID2022-141553OB-I0（FEDER/EU）资助；La Caixa基金会（ID 100010434），根据协议LCF/PR/HR17，Fundación Cris Contra el Cáncer（PR\U EX\U 2021-22），Severo Ochoa卓越认证CEX2021-001136-S），2023年阿斯利康肿瘤学青年科学家奖，欧洲培训网络项目（H2020-MSCA-ITN-308 2016 721532），Vencer el Cáncer基金会，iDIFFER卓越网络（RED2022-134792-T），Asociación Española Contra el Cáncer（GCTRA18006CARR））和欧洲研究理事会（Consolidator Grant 819242）。

L. Bozal was supported by the AECC Foundation (POSTD19048BOZA). CIBERONC was co-funded with FEDER funds and funded by ISCIII.Author informationAuthors and AffiliationsCenter for Cooperative Research in Biosciences (CIC bioGUNE), Basque Research and Technology Alliance (BRTA), Bizkaia Technology Park, Building 801A, 48160, Derio, SpainMikel Pujana-Vaquerizo, Laura Bozal-Basterra & Arkaitz CarracedoCentro de Investigación Biomédica En Red de Cáncer (CIBERONC), 28029, Madrid, SpainMikel Pujana-Vaquerizo & Arkaitz CarracedoTraslational Prostate Cancer Research Lab, CIC bioGUNE-Basurto, Biobizkaia Health Research Institute, Baracaldo, SpainArkaitz CarracedoIkerbasque, Basque Foundation for Science, Bilbao, SpainArkaitz CarracedoBiochemistry and Molecular Biology Department, University of the Basque Country (UPV/EHU), Leioa, SpainArkaitz CarracedoAuthorsMikel Pujana-VaquerizoView author publicationsYou can also search for this author in.

五十、 Bozal得到了AECC基金会（POSTD19048BOZA）的支持。CIBERONC与FEDER基金共同资助，并由ISCIII资助。作者信息作者和附属机构生物科学合作研究中心（CIC bioGUNE），巴斯克研究与技术联盟（BRTA），Bizkaia科技园，801A栋，48160，Derio，SpainMikel Pujana Vaquerizo，Laura Bozal Basterra＆Arkaitz CarracedoCentro de Investigación Biomédica En Red de Cáncer（CIBERONC），28029，马德里，SpainMikel Pujana Vaquerizo＆Arkaitz CarracedoTraslational前列腺癌研究实验室，CIC bioGUNE Basurto，Biobizkaia Health Research Institute，Barabara Caldo，SpainArkaitz CarracedoIkerbasque，巴斯克科学基金会，毕尔巴鄂，SpainArkaitz Carracedoidobiochemistry and Molecular Biology Department，巴斯克国家大学（UPV/EHU），Leioa，SpainArkaitz CarracedoAuthorsMikel Pujana VaquerizoView Author Publications你也可以在中搜索这位作者。

PubMed Google ScholarLaura Bozal-BasterraView author publicationsYou can also search for this author in

PubMed Google ScholarLaura Bozal BasterraView作者出版物您也可以在

PubMed Google ScholarArkaitz CarracedoView author publicationsYou can also search for this author in

PubMed Google ScholarArkaitz CarracedoView作者出版物您也可以在

PubMed Google ScholarContributionsMP performed bibliography search, contributed to structuring the review, preparing the figures and writing specific sections of the manuscript. LB coordinated the design of the review with AC, performed bibliography search, contributed to structuring the review, preparing the figures and writing sections of the manuscript.

PubMed Google ScholarContributionsMP进行了书目搜索，为构建评论，准备数字和撰写稿件的特定部分做出了贡献。LB与AC协调了评论的设计，进行了书目搜索，为构建评论，准备数字和撰写稿件做出了贡献。

AC supervised the structure, design and writing of the review, and perform critical reading and editing of the manuscript.Corresponding authorsCorrespondence to.

AC监督审查的结构，设计和撰写，并对稿件进行批判性阅读和编辑。通讯作者通讯。

Laura Bozal-Basterra or Arkaitz Carracedo.Ethics declarations

劳拉·博扎尔·巴斯特拉（LauraBozalBasterra）或阿尔凯茨·卡拉塞多（ArkaitzCarracedo）。道德宣言

Competing interests

相互竞争的利益

The authors declare no competing interests.

作者声明没有利益冲突。

Additional informationPublisher’s note Springer Nature remains neutral with regard to jurisdictional claims in published maps and institutional affiliations.Rights and permissions

Additional informationPublisher的注释Springer Nature在已发布的地图和机构隶属关系中的管辖权主张方面保持中立。权限和权限

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made.

开放获取本文是根据知识共享署名4.0国际许可证授权的，该许可证允许以任何媒体或格式使用，共享，改编，分发和复制，只要您对原始作者和来源给予适当的信任，提供知识共享许可证的链接，并指出是否进行了更改。

The images or other third party material in this article are included in the article’s Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder.

本文中的图像或其他第三方材料包含在文章的知识共享许可中，除非在材料的信用额度中另有说明。如果材料未包含在文章的知识共享许可中，并且您的预期用途不受法律法规的许可或超出许可用途，则您需要直接获得版权所有者的许可。

To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/..

要查看此许可证的副本，请访问http://creativecommons.org/licenses/by/4.0/..

Reprints and permissionsAbout this articleCite this articlePujana-Vaquerizo, M., Bozal-Basterra, L. & Carracedo, A. Metabolic adaptations in prostate cancer.

转载和许可本文引用本文Pujana Vaquerizo，M.，Bozal Basterra，L。＆Carracedo，A。前列腺癌的代谢适应。

Br J Cancer (2024). https://doi.org/10.1038/s41416-024-02762-zDownload citationReceived: 13 March 2024Revised: 07 June 2024Accepted: 11 June 2024Published: 05 July 2024DOI: https://doi.org/10.1038/s41416-024-02762-zShare this articleAnyone you share the following link with will be able to read this content:Get shareable linkSorry, a shareable link is not currently available for this article.Copy to clipboard.

Br J癌症（2024）。https://doi.org/10.1038/s41416-024-02762-zDownload引文收到日期：2024年3月13日修订日期：2024年6月7日接受日期：2024年6月11日发布日期：2024年7月5日OI：https://doi.org/10.1038/s41416-024-02762-zShare本文与您共享以下链接的任何人都可以阅读此内容：获取可共享链接对不起，本文目前没有可共享的链接。。

Provided by the Springer Nature SharedIt content-sharing initiative

由Springer Nature SharedIt内容共享计划提供