癌症中的SMYD家族：癌症增殖、转移和耐药性的表观遗传学调控及其分子机制-动脉网

SMYD family in cancer: epigenetic regulation and molecular mechanisms of cancer proliferation, metastasis, and drug resistance

Nature 等信源发布 2024-11-01 13:50

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AbstractEpigenetic modifiers (miRNAs, histone methyltransferases (HMTs)/demethylases, and DNA methyltransferases/demethylases) are associated with cancer proliferation, metastasis, angiogenesis, and drug resistance. Among these modifiers, HMTs are frequently overexpressed in various cancers, and recent studies have increasingly identified these proteins as potential therapeutic targets.

。在这些修饰剂中，HMT经常在各种癌症中过度表达，最近的研究越来越多地将这些蛋白质鉴定为潜在的治疗靶标。

In this review, we discuss members of the SET and MYND domain-containing protein (SMYD) family that are topics of extensive research on the histone methylation and nonhistone methylation of cancer-related genes. Various members of the SMYD family play significant roles in cancer proliferation, metastasis, and drug resistance by regulating cancer-specific histone methylation and nonhistone methylation.

在这篇综述中，我们讨论了SET和MYND结构域蛋白（SMYD）家族的成员，这些成员是癌症相关基因组蛋白甲基化和非组蛋白甲基化的广泛研究主题。SMYD家族的各个成员通过调节癌症特异性组蛋白甲基化和非组蛋白甲基化在癌症增殖，转移和耐药性中发挥重要作用。

Thus, the development of specific inhibitors that target SMYD family members may lead to the development of cancer treatments, and combination therapy with various anticancer therapeutic agents may increase treatment efficacy..

因此，针对SMYD家族成员的特异性抑制剂的开发可能会导致癌症治疗的发展，与各种抗癌治疗剂的联合治疗可能会提高治疗效果。。

IntroductionEpigenetic processes play crucial roles in various stages of cancer growth. DNA methylation, histone modification (including methylation, acetylation, phosphorylation, and ubiquitylation), and microRNAs (miRNAs) are associated with the regulation of oncogene and tumor suppressor gene expression1,2,3,4.

引言表观遗传过程在癌症生长的各个阶段起着至关重要的作用。DNA甲基化，组蛋白修饰（包括甲基化，乙酰化，磷酸化和泛素化）和microRNA（miRNA）与癌基因和抑癌基因表达的调节有关1,2,3,4。

Recently, through public databases such as The Cancer Genome Atlas (TCGA) database, it has been observed that the expression levels of epigenetic modifiers are up- or downregulated in cancer cells, suggesting their involvement in cancer-related processes5,6,7.Among epigenetic modifiers, histone methyltransferases (HMTs), which are responsible for histone methylation in cancer-related epigenetic processes, are involved in regulating the expression of various oncogenes and tumor suppressor genes by altering euchromatin and heterochromatin structures8.

最近，通过癌症基因组图谱（TCGA）数据库等公共数据库，已经观察到表观遗传修饰因子的表达水平在癌细胞中上调或下调，表明它们参与癌症相关过程5,6,7。在表观遗传修饰因子中，组蛋白甲基转移酶（HMTs）负责癌症相关表观遗传过程中的组蛋白甲基化，通过改变常染色质和异染色质结构参与调节各种癌基因和肿瘤抑制基因的表达8。

Consequently, the expression of genes related to cancer growth, metastasis, and chemotherapy resistance is regulated by HMTs, making these enzymes potential therapeutic targets for cancer treatment9. In recent developments in cancer therapy, specific inhibitors, such as tazemetostat, which targets enhancer of zeste homolog 2 (EZH2) and thereby mediates histone H3 lysine (K) 27 methylation, have been approved by the Food and Drug Administration (FDA) for the treatment of follicular lymphoma and are currently in use.

因此，与癌症生长，转移和化疗耐药相关的基因的表达受HMT调控，使这些酶成为癌症治疗的潜在治疗靶点9。在癌症治疗的最新发展中，美国食品和药物管理局（FDA）已批准用于治疗滤泡性淋巴瘤的特异性抑制剂，例如靶向zeste同源物2（EZH2）增强子的tazemetostat，从而介导组蛋白H3赖氨酸（K）27甲基化，目前正在使用中。

Moreover, various clinical studies are being conducted to explore the possibility of applying these inhibitors to treat different cancers10. The successful development of EZH2 inhibitors has led to active research on the mechanisms by which various HMTs function, and these studies have shown that HMTs have potential for use as crucial targets for cancer treatment.Therefore, the aim of this review was to .

此外，正在进行各种临床研究，以探索应用这些抑制剂治疗不同癌症的可能性10。EZH2抑制剂的成功开发导致了对各种HMT功能机制的积极研究，这些研究表明HMT有潜力用作癌症治疗的关键靶标。因此，这次审查的目的是。

ReferencesLee, J. et al. Positive regulation of cell proliferation by the miR-1290-EHHADH axis in hepatocellular carcinoma. Cancer Commun. https://doi.org/10.1002/cac2.12536 (2024).Li, L., Song, Q., Zhou, J. & Ji, Q. Controllers of histone methylation-modifying enzymes in gastrointestinal cancers. Biomed.

参考文献Lee，J。等人。miR-1290-EHHADH轴对肝细胞癌细胞增殖的正调控。癌症社区。https://doi.org/10.1002/cac2.12536（2024年）。Li，L.，Song，Q.，Zhou，J。＆Ji，Q。胃肠道癌症中组蛋白甲基化修饰酶的控制者。生物医学。

Pharmacother. 174, 116488 (2024).Article .

药剂师。174116488（2024）。文章。

PubMed

CAS

中科院

Google Scholar

谷歌学者

Sriharikrishnaa, S. et al. A comprehensive review on the functional role of miRNA clusters in cervical cancer. Epigenomics 16, 493–511 (2024).Article

Sriharikrishnaa，S.等。关于miRNA簇在宫颈癌中的功能作用的综合综述。表观基因组学16493-511（2024）。文章

PubMed

CAS

中科院

Google Scholar

谷歌学者

Zhao, N., Lai, C., Wang, Y., Dai, S. & Gu, H. Understanding the role of DNA methylation in colorectal cancer: mechanisms, detection, and clinical significance. Biochim. Biophys. Acta Rev. Cancer 189096 https://doi.org/10.1016/j.bbcan.2024.189096 (2024).Kim, K. et al. Epigenetic silencing of CHOP expression by the histone methyltransferase EHMT1 regulates apoptosis in colorectal cancer cells.

Zhao，N.，Lai，C.，Wang，Y.，Dai，S。＆Gu，H。了解DNA甲基化在结直肠癌中的作用：机制，检测和临床意义。。生物物理。癌症学报189096https://doi.org/10.1016/j.bbcan.2024.189096（2024年）。Kim，K。等人。组蛋白甲基转移酶EHMT1对CHOP表达的表观遗传沉默调节结直肠癌细胞的凋亡。

Mol. Cells 45, 622–630 (2022).Article .

分子细胞45622-630（2022）。文章。

PubMed

PubMed Central

公共医学中心

CAS

中科院

Google Scholar

谷歌学者

Ryu, T. Y. et al. Human gut-microbiome-derived propionate coordinates proteasomal degradation via HECTD2 upregulation to target EHMT2 in colorectal cancer. ISME J. 16, 1205–1221 (2022).Article

Ryu，T.Y.等人。人类肠道微生物组衍生的丙酸盐通过HECTD2上调来协调蛋白酶体降解，从而靶向结直肠癌中的EHMT2。ISME J.161205–1221（2022）。文章

PubMed

PubMed Central

公共医学中心

CAS

中科院

Google Scholar

谷歌学者

Ryu, T. Y. et al. Epigenetic regulation of DHRS2 by SUV420H2 inhibits cell apoptosis in renal cell carcinoma. Biochem. Biophys. Res. Commun. 663, 41–46 (2023).Article

。生物化学。生物物理。公共资源。663,41-46（2023）。文章

PubMed

CAS

中科院

Google Scholar

谷歌学者

Bannister, A. J. & Kouzarides, T. Regulation of chromatin by histone modifications. Cell Res. 21, 381–395 (2011).Article

Bannister，A.J。＆Kouzarides，T。通过组蛋白修饰调节染色质。Cell Res.21381–395（2011）。文章

PubMed

PubMed Central

公共医学中心

CAS

中科院

Google Scholar

谷歌学者

Chen, Y. et al. The role of histone methylation in the development of digestive cancers: a potential direction for cancer management. Signal. Transduct. Target Ther. 5, 143 (2020).Article

Chen，Y.等人。组蛋白甲基化在消化系统癌症发展中的作用：癌症管理的潜在方向。。Transduct公司。目标Ther。5143（2020）。文章

PubMed

PubMed Central

公共医学中心

CAS

中科院

Google Scholar

谷歌学者

Marzochi, L. L. et al. Use of histone methyltransferase inhibitors in cancer treatment: a systematic review. Eur. J. Pharm. 944, 175590 (2023).Article

Marzochi，L.L.等人。组蛋白甲基转移酶抑制剂在癌症治疗中的应用：系统综述。《欧洲药典》944175590（2023）。文章

CAS

中科院

Google Scholar

谷歌学者

Padilla, A. et al. Targeting epigenetic changes mediated by members of the SMYD family of lysine methyltransferases. Molecules 28 https://doi.org/10.3390/molecules28042000 (2023).Tracy, C. et al. The Smyd family of methyltransferases: role in cardiac and skeletal muscle physiology and pathology.

Padilla，A。等人。针对赖氨酸甲基转移酶SMYD家族成员介导的表观遗传变化。分子28https://doi.org/10.3390/molecules28042000（2023年）。Tracy，C.等人。Smyd甲基转移酶家族：在心肌和骨骼肌生理和病理学中的作用。

Curr. Opin. Physiol. 1, 140–152 (2018).Article .

货币。奥平。生理学。1140-152（2018）。文章。

PubMed

Google Scholar

谷歌学者

Liu, D. et al. SMYD family members serve as potential prognostic markers and correlate with immune infiltrates in gastric cancer. J. Oncol. 2023, 6032864 (2023).Article

Liu，D。等人。SMYD家族成员可作为潜在的预后标志物，并与胃癌的免疫浸润相关。J、 Oncol公司。20236032864（2023）。文章

PubMed

PubMed Central

公共医学中心

Google Scholar

谷歌学者

Nation, J. B., Cabot-Miller, J., Segal, O., Lucito, R. & Adaricheva, K. Combining algorithms to find signatures that predict risk in early-stage stomach cancer. J. Comput. Biol. 28, 985–1006 (2021).Article

Nation，J.B.，Cabot-Miller，J.，Segal，O.，Lucito，R。＆Adaricheva，K。结合算法找到预测早期胃癌风险的特征。J、计算机。生物学28985-1006（2021）。文章

PubMed

CAS

中科院

Google Scholar

谷歌学者

Song, J. et al. Expression patterns and the prognostic value of the SMYD family members in human breast carcinoma using integrative bioinformatics analysis. Oncol. Lett. 17, 3851–3861 (2019).PubMed

Song，J。等人。使用综合生物信息学分析，SMYD家族成员在人乳腺癌中的表达模式和预后价值。Oncol公司。利特。173851-3861（2019）。PubMed出版社

PubMed Central

公共医学中心

CAS

中科院

Google Scholar

谷歌学者

Zhang, Y. et al. Integrated analysis of genetic abnormalities of the histone lysine methyltransferases in prostate cancer. Med. Sci. Monit. 25, 193–239 (2019).Article

Zhang，Y。等。前列腺癌组蛋白赖氨酸甲基转移酶遗传异常的综合分析。医学科学。莫尼特。25193-239（2019）。文章

PubMed

PubMed Central

公共医学中心

CAS

中科院

Google Scholar

谷歌学者

Shi, W. et al. CHD4 and SMYD1 repress common transcriptional programs in the developing heart. Development 151 https://doi.org/10.1242/dev.202505 (2024).Chen, M., Li, J., Wang, J., Le, Y. & Liu, C. SMYD1 alleviates septic myocardial injury by inhibiting endoplasmic reticulum stress. Biosci.

Shi，W。等人，CHD4和SMYD1抑制发育中心脏中的常见转录程序。发展151https://doi.org/10.1242/dev.202505（2024年）。Chen，M.，Li，J.，Wang，J.，Le，Y。＆Liu，C。SMYD1通过抑制内质网应激来减轻脓毒性心肌损伤。。

Biotechnol. Biochem. 85, 2383–2391 (2021).Article .

生物技术。生物化学。85, 2383-2391 (2021).第[UNK]条。

PubMed

Google Scholar

谷歌学者

Tang, J. et al. Resistance training up-regulates Smyd1 expression and inhibits oxidative stress and endoplasmic reticulum stress in the heart of middle-aged mice. Free Radic. Biol. Med. 210, 304–317 (2024).Article

Tang，J。等人。阻力训练上调Smyd1的表达，并抑制中年小鼠心脏中的氧化应激和内质网应激。自由基。生物医学210304-317（2024）。文章

PubMed

CAS

中科院

Google Scholar

谷歌学者

Singh, S. et al. Musashi-2 causes cardiac hypertrophy and heart failure by inducing mitochondrial dysfunction through destabilizing Cluh and Smyd1 mRNA. Basic Res. Cardiol. 118, 46 (2023).Article

Singh，S。等人。Musashi-2通过使Cluh和Smyd1 mRNA不稳定而诱导线粒体功能障碍，从而导致心脏肥大和心力衰竭。基础研究。Cardiol。118，46（2023）。文章

PubMed

CAS

中科院

Google Scholar

谷歌学者

Zheng, C. et al. Dynamic transcriptome profiles of skeletal muscle growth and development in Shaziling and Yorkshire pigs using RNA-sequencing. J. Sci. Food Agric. https://doi.org/10.1002/jsfa.13551 (2024).Zhu, L. et al. Lysine methyltransferase SMYD1 regulates myogenesis via skNAC methylation.

郑，C。等。使用RNA测序对沙子岭猪和约克郡猪骨骼肌生长和发育的动态转录组谱。J、科学。粮食农业。https://doi.org/10.1002/jsfa.13551（2024年）。Zhu，L。等人。赖氨酸甲基转移酶SMYD1通过skNAC甲基化调节肌生成。

Cells 12 https://doi.org/10.3390/cells12131695 (2023).Li, F. et al. Down-regulated Smyd1 participated in the inhibition of myoblast differentiation induced by cigarette smoke extract. Toxicol. Lett. 383, 98–111 (2023).Article .

单元格12https://doi.org/10.3390/cells12131695（2023年）。Li，F。等人下调Smyd1参与抑制香烟烟雾提取物诱导的成肌细胞分化。毒理学。利特。383、98-111（2023）。文章。

PubMed

CAS

中科院

Google Scholar

谷歌学者

Yi, X., Jiang, X. J. & Fang, Z. M. Histone methyltransferase SMYD2: ubiquitous regulator of disease. Clin. Epigenetics 11, 112 (2019).Article

Yi，X.，Jiang，X。J。和Fang，Z。M。组蛋白甲基转移酶SMYD2：无处不在的疾病调节剂。临床。表观遗传学11112（2019）。文章

PubMed

PubMed Central

公共医学中心

Google Scholar

谷歌学者

Li, L. X. et al. Lysine methyltransferase SMYD2 promotes triple negative breast cancer progression. Cell Death Dis. 9, 326 (2018).Article

Li，L.X。等人。赖氨酸甲基转移酶SMYD2促进三阴性乳腺癌进展。细胞死亡Dis。9326（2018）。文章

PubMed

PubMed Central

公共医学中心

Google Scholar

谷歌学者

Yadav, A. K. & Singh, T. R. Computational approach for assessing the involvement of SMYD2 protein in human cancers using TCGA data. J. Genet. Eng. Biotechnol. 21, 122 (2023).Article

Yadav，A.K。＆Singh，T.R。使用TCGA数据评估SMYD2蛋白在人类癌症中的参与的计算方法。J、基因。工程生物技术。。文章

PubMed

PubMed Central

公共医学中心

Google Scholar

谷歌学者

Xu, Z., Liu, Y., Pan, Z. & Qin, L. Epigenetic upregulation of MNAT1 by SMYD2 is linked to PI3K/AKT activation and tumorigenesis of pancreatic adenocarcinoma. Histol. Histopathol. 39, 263–277 (2024).PubMed

Xu，Z.，Liu，Y.，Pan，Z。＆Qin，L。SMYD2对MNAT1的表观遗传上调与PI3K/AKT活化和胰腺癌的肿瘤发生有关。历史。组织病理学。39263-277（2024）。PubMed出版社

CAS

中科院

Google Scholar

谷歌学者

Li, J. et al. Targeting SMYD2 inhibits prostate cancer cell growth by regulating c-Myc signaling. Mol. Carcinog. 62, 940–950 (2023).Article

Li，J。等人。靶向SMYD2通过调节c-Myc信号传导抑制前列腺癌细胞生长。分子癌症。62940-950（2023）。文章

PubMed

CAS

中科院

Google Scholar

谷歌学者

Lai, Y. & Yang, Y. SMYD2 facilitates cancer cell malignancy and xenograft tumor development through ERBB2-mediated FUT4 expression in colon cancer. Mol. Cell Biochem. 477, 2149–2159 (2022).Article

Lai，Y。＆Yang，Y。SMYD2通过ERBB2介导的结肠癌中FUT4的表达促进癌细胞恶性肿瘤和异种移植肿瘤的发展。分子细胞生物化学。4772149-2159（2022）。文章

PubMed

CAS

中科院

Google Scholar

谷歌学者

Pan, L., Fan, Y. & Zhou, L. SMYD2 epigenetically activates MEX3A and suppresses CDX2 in colorectal cancer cells to augment cancer growth. Clin. Exp. Pharm. Physiol. 49, 959–969 (2022).Article

Pan，L.，Fan，Y。＆Zhou，L。SMYD2表观遗传学激活MEX3A并抑制结直肠癌细胞中的CDX2以增强癌症生长。临床。实验药物生理学。49959-969（2022）。文章

CAS

中科院

Google Scholar

谷歌学者

Aravena, T. I., Valdes, E., Ayala, N. & D’Afonseca, V. A computational approach to predict the role of genetic alterations in methyltransferase histones genes with implications in liver cancer. Cancer Inf. 22, 11769351231161480 (2023).

Aravena，T.I.，Valdes，E.，Ayala，N。＆D'Afonseca，V。一种预测甲基转移酶组蛋白基因遗传改变在肝癌中的作用的计算方法。癌症信息221769351231480（2023）。

Google Scholar

谷歌学者

Kojima, M. et al. The histone methyltransferase SMYD2 is a novel therapeutic target for the induction of apoptosis in ovarian clear cell carcinoma cells. Oncol. Lett. 20, 153 (2020).Article

组蛋白甲基转移酶SMYD2是诱导卵巢透明细胞癌细胞凋亡的新型治疗靶点。Oncol公司。利特。20153（2020）。文章

PubMed

PubMed Central

公共医学中心

CAS

中科院

Google Scholar

谷歌学者

Li, X., Wang, Y., Zhang, Y. & Liu, B. Overexpression of MCAM induced by SMYD2-H3K36me2 in breast cancer stem cell properties. Breast Cancer 29, 854–868 (2022).Article

Li，X.，Wang，Y.，Zhang，Y。＆Liu，B.SMYD2-H3K36me2诱导的MCAM在乳腺癌干细胞特性中的过表达。乳腺癌29854-868（2022）。文章

PubMed

Google Scholar

谷歌学者

Pan, K., Hu, B., Wang, L., Yuan, J. & Xu, W. STUB1-SMYD2 axis regulates drug resistance in glioma cells. J. Mol. Neurosci. 72, 2030–2044 (2022).Article

Pan，K.，Hu，B.，Wang，L.，Yuan，J。＆Xu，W。STUB1-SMYD2轴调节胶质瘤细胞的耐药性。J、分子神经科学。722030年至2044年（2022年）。文章

PubMed

CAS

中科院

Google Scholar

谷歌学者

Brown, M. A. et al. The lysine methyltransferase SMYD2 is required for normal lymphocyte development and survival of hematopoietic leukemias. Genes Immun. 21, 119–130 (2020).Article

Brown，M.A.等人。赖氨酸甲基转移酶SMYD2是正常淋巴细胞发育和造血白血病存活所必需的。基因免疫。21119-130（2020）。文章

PubMed

PubMed Central

公共医学中心

CAS

中科院

Google Scholar

谷歌学者

Zhang, P., Ruan, J., Weng, W. & Tang, Y. Overexpression of SET and MYND domain-containing protein 2 (SMYD2) is associated with poor prognosis in pediatric B lineage acute lymphoblastic leukemia. Leuk. Lymphoma 61, 437–444 (2020).Article

Zhang，P.，Ruan，J.，Weng，W。＆Tang，Y。SET和MYND结构域蛋白2（SMYD2）的过表达与小儿B系急性淋巴细胞白血病的预后不良有关。白血病。淋巴瘤61437-444（2020）。文章

PubMed

CAS

中科院

Google Scholar

谷歌学者

Sun, J. J. et al. SMYD2 promotes cervical cancer growth by stimulating cell proliferation. Cell Biosci. 9, 75 (2019).Article

Sun，J。J。等人。SMYD2通过刺激细胞增殖促进宫颈癌的生长。。9，75（2019）。文章

PubMed

PubMed Central

公共医学中心

Google Scholar

谷歌学者

Yan, L. et al. Inhibition of SMYD2 suppresses tumor progression by down-regulating microRNA-125b and attenuates multi-drug resistance in renal cell carcinoma. Theranostics 9, 8377–8391 (2019).Article

Yan，L。等人。抑制SMYD2通过下调microRNA-125b抑制肿瘤进展，并减弱肾细胞癌的多药耐药性。Theranostics 98377-8391（2019）。文章

PubMed

PubMed Central

公共医学中心

CAS

中科院

Google Scholar

谷歌学者

Xu, K. et al. SMYD2 promotes hepatocellular carcinoma progression by reprogramming glutamine metabolism via c-Myc/GLS1 axis. Cells 12 https://doi.org/10.3390/cells12010025 (2022).Yu, Y. Q. et al. SMYD2 targets RIPK1 and restricts TNF-induced apoptosis and necroptosis to support colon tumor growth.

Xu，K。等人。SMYD2通过c-Myc/GLS1轴重编程谷氨酰胺代谢来促进肝细胞癌的进展。单元格12https://doi.org/10.3390/cells12010025（2022年）。Yu，Y。Q。等人，SMYD2靶向RIPK1并限制TNF诱导的细胞凋亡和坏死性凋亡以支持结肠肿瘤生长。

Cell Death Dis. 13, 52 (2022).Article .

细胞死亡Dis。13，52（2022）。文章。

PubMed

PubMed Central

公共医学中心

CAS

中科院

Google Scholar

谷歌学者

Zhang, Y. et al. Targeting SMYD2 inhibits angiogenesis and increases the efficiency of apatinib by suppressing EGFL7 in colorectal cancer. Angiogenesis 26, 1–18 (2023).Article

Zhang，Y。等人。靶向SMYD2通过抑制结直肠癌中的EGFL7来抑制血管生成并提高阿帕替尼的效率。血管生成26,1-18（2023）。文章

PubMed

Google Scholar

谷歌学者

Meng, F. et al. SMYD2 suppresses APC2 expression to activate the Wnt/beta-catenin pathway and promotes epithelial-mesenchymal transition in colorectal cancer. Am. J. Cancer Res. 10, 997–1011 (2020).PubMed

Meng，F。等人。SMYD2抑制APC2表达以激活Wnt/β-连环蛋白途径并促进结直肠癌的上皮-间质转化。《美国癌症杂志》第10997-1011号（2020年）。PubMed出版社

PubMed Central

公共医学中心

CAS

中科院

Google Scholar

谷歌学者

Wang, Y. et al. SMYD2 suppresses p53 activity to promote glucose metabolism in cervical cancer. Exp. Cell Res. 404, 112649 (2021).Article

Wang，Y。等人。SMYD2抑制p53活性以促进宫颈癌中的葡萄糖代谢。Exp.Cell Res.404112649（2021）。文章

PubMed

CAS

中科院

Google Scholar

谷歌学者

Casanova, A. G. et al. Cytoskeleton remodeling induced by SMYD2 methyltransferase drives breast cancer metastasis. Cell Discov. 10, 12 (2024).Article

Casanova，A.G.等人。SMYD2甲基转移酶诱导的细胞骨架重塑驱动乳腺癌转移。细胞Discov。10、12（2024年）。文章

PubMed

PubMed Central

公共医学中心

CAS

中科院

Google Scholar

谷歌学者

Kim, K. et al. Epigenetic regulation of SMAD3 by histone methyltransferase SMYD2 promotes lung cancer metastasis. Exp. Mol. Med. 55, 952–964 (2023).Article

Kim，K。等人。组蛋白甲基转移酶SMYD2对SMAD3的表观遗传调控促进肺癌转移。实验分子医学55952-964（2023）。文章

PubMed

PubMed Central

公共医学中心

CAS

中科院

Google Scholar

谷歌学者

Wu, L. et al. SMYD2 promotes tumorigenesis and metastasis of lung adenocarcinoma through RPS7. Cell Death Dis. 12, 439 (2021).Article

Wu，L。等人。SMYD2通过RPS7促进肺腺癌的肿瘤发生和转移。细胞死亡Dis。12439（2021）。文章

PubMed

PubMed Central

公共医学中心

CAS

中科院

Google Scholar

谷歌学者

Munawwar, A., Sajjad, A., Rasul, A., Sattar, M. & Jabeen, F. Dissecting the role of SMYD2 and its inhibitor (LLY-507) in the treatment of chemically induced non-small cell lung cancer (NSCLC) by using Fe(3)O(4) nanoparticles drug delivery system. Pharmaceuticals 16 https://doi.org/10.3390/ph16070986 (2023).Zhang, B.

Munawwar，A.，Sajjad，A.，Rasul，A.，Sattar，M。＆Jabeen，F。剖析SMYD2及其抑制剂（LLY-507）在化学诱导的非小细胞肺癌（NSCLC）治疗中的作用）通过使用Fe（3）O（4）纳米颗粒药物递送系统。制药16https://doi.org/10.3390/ph16070986（2023年）。张，B。

et al. Synthesis and structure-activity relationship studies of LLY-507 analogues as SMYD2 inhibitors. Bioorg. Med. Chem. Lett. 30, 127598 (2020).Article .

LLY-507类似物作为SMYD2抑制剂的合成和构效关系研究。生物组织医学化学。利特。30127598（2020）。文章。

PubMed

CAS

中科院

Google Scholar

谷歌学者

Kukita, A. et al. Histone methyltransferase SMYD2 selective inhibitor LLY-507 in combination with poly ADP ribose polymerase inhibitor has therapeutic potential against high-grade serous ovarian carcinomas. Biochem. Biophys. Res. Commun. 513, 340–346 (2019).Article

Kukita，A。等人。组蛋白甲基转移酶SMYD2选择性抑制剂LLY-507与聚ADP-核糖聚合酶抑制剂联合对高度浆液性卵巢癌具有治疗潜力。生物化学。生物物理。公共资源。513340-346（2019）。文章

PubMed

CAS

中科院

Google Scholar

谷歌学者

Siddique, A. B. et al. Oleocanthal attenuates metastatic castration-resistant prostate cancer progression and recurrence by targeting SMYD2. Cancers 14 https://doi.org/10.3390/cancers14143542 (2022).Gu, L., Xu, F., Zhang, X. & Gu, Z. Baicalein Inhibits the SMYD2/RPS7 signaling pathway to inhibit the occurrence and metastasis of lung cancer.

Siddique，A.B.等人，Oleocanthal通过靶向SMYD2来减弱转移性去势抵抗性前列腺癌的进展和复发。癌症14https://doi.org/10.3390/cancers14143542（2022年）。Gu，L.，Xu，F.，Zhang，X。＆Gu，Z。黄芩素抑制SMYD2/RPS7信号通路以抑制肺癌的发生和转移。

J. Oncol. 2022, 3796218 (2022).Article .

J、肿瘤。20223796218（2022）。文章。

PubMed

PubMed Central

公共医学中心

Google Scholar

谷歌学者

Fang, W. et al. Effect of miRNA-200b on the proliferation of liver cancer cells via targeting SMYD2/p53 signaling pathway. Zhong Nan Da Xue Xue Bao Yi Xue Ban. 47, 1303–1314 (2022).PubMed

Fang，W。等人。miRNA-200b通过靶向SMYD2/p53信号通路对肝癌细胞增殖的影响。中南大学学报医学版。471303-1314（2022）。PubMed出版社

Google Scholar

谷歌学者

Yu, H., Zhang, D. & Lian, M. Identification of an epigenetic prognostic signature for patients with lower-grade gliomas. CNS Neurosci. Ther. 27, 470–483 (2021).Article

Yu，H.，Zhang，D。＆Lian，M。鉴定低级别胶质瘤患者的表观遗传预后特征。中枢神经系统神经科学。他们。27470–483（2021）。文章

PubMed

PubMed Central

公共医学中心

CAS

中科院

Google Scholar

谷歌学者

Engqvist, H. et al. Validation of novel prognostic biomarkers for early-stage clear-cell, endometrioid and mucinous ovarian carcinomas using immunohistochemistry. Front. Oncol. 10, 162 (2020).Article

Engqvist，H。等人。使用免疫组织化学验证早期透明细胞癌，子宫内膜样癌和粘液性卵巢癌的新型预后生物标志物。正面。Oncol公司。10162（2020）。文章

PubMed

PubMed Central

公共医学中心

Google Scholar

谷歌学者

Tan, Z. et al. Identification of potential biomarkers for progression and prognosis of bladder cancer by comprehensive bioinformatics analysis. J. Oncol. 2022, 1802706 (2022).Article

Tan，Z.等人。通过综合生物信息学分析鉴定膀胱癌进展和预后的潜在生物标志物。J、 Oncol公司。20221802706（2022）。文章

PubMed

PubMed Central

公共医学中心

Google Scholar

谷歌学者

Wang, N., Ma, T. & Yu, B. Targeting epigenetic regulators to overcome drug resistance in cancers. Signal. Transduct. Target Ther. 8, 69 (2023).Article

Wang，N.，Ma，T。＆Yu，B。靶向表观遗传调节剂以克服癌症的耐药性。。Transduct公司。目标Ther。8，69（2023）。文章

PubMed

PubMed Central

公共医学中心

CAS

中科院

Google Scholar

谷歌学者

Li, J. et al. Lysine methyltransferase SMYD2 enhances androgen receptor signaling to modulate CRPC cell resistance to enzalutamide. Oncogene 43, 744–757 (2024).Article

Li，J。等人。赖氨酸甲基转移酶SMYD2增强雄激素受体信号传导以调节CRPC细胞对恩扎鲁胺的抗性。癌基因43744-757（2024）。文章

PubMed

CAS

中科院

Google Scholar

谷歌学者

Shang, L. & Wei, M. Inhibition of SMYD2 sensitized cisplatin to resistant cells in NSCLC through activating p53 pathway. Front. Oncol. 9, 306 (2019).Article

Shang，L。＆Wei，M。通过激活p53途径抑制SMYD2使顺铂对NSCLC中的耐药细胞敏感。正面。Oncol公司。9306（2019）。文章

PubMed

PubMed Central

公共医学中心

Google Scholar

谷歌学者

Ren, H. et al. SMYD2-OE promotes oxaliplatin resistance in colon cancer through MDR1/P-glycoprotein via MEK/ERK/AP1 pathway. Onco Targets Ther. 12, 2585–2594 (2019).Article

Ren，H。等人。SMYD2-OE通过MEK/ERK/AP1途径通过MDR1/P-糖蛋白促进结肠癌对奥沙利铂的耐药性。Onco以Ther为目标。122585-2594（2019）。文章

PubMed

PubMed Central

公共医学中心

CAS

中科院

Google Scholar

谷歌学者

Dashti, P. et al. Epigenetic regulators controlling osteogenic lineage commitment and bone formation. Bone 181, 117043 (2024).Article

Dashti，P。等人。控制成骨谱系承诺和骨形成的表观遗传调节剂。骨181117043（2024）。文章

PubMed

CAS

中科院

Google Scholar

谷歌学者

Dashti, P. et al. The lysine methyltransferases SET and MYND domain containing 2 (Smyd2) and Enhancer of Zeste 2 (Ezh2) co-regulate osteoblast proliferation and mineralization. Gene 851, 146928 (2023).Article

Dashti，P。等人。赖氨酸甲基转移酶SET和含有2（Smyd2）的MYND结构域和Zeste 2（Ezh2）的增强子共同调节成骨细胞的增殖和矿化。基因851146928（2023）。文章

PubMed

CAS

中科院

Google Scholar

谷歌学者

Su, Z. et al. Histone methyltransferase Smyd2 drives vascular aging by its enhancer-dependent activity. Aging 15, 70–91 (2022).Article

Su，Z。等人。组蛋白甲基转移酶Smyd2通过其增强子依赖性活性驱动血管衰老。15岁，70-91岁（2022年）。文章

PubMed

PubMed Central

公共医学中心

Google Scholar

谷歌学者

Wang, J. et al. Histone methyltransferase Smyd2 contributes to blood-brain barrier breakdown in stroke. Clin. Transl. Med. 12, e761 (2022).Article

Wang，J。等人。组蛋白甲基转移酶Smyd2有助于中风的血脑屏障破坏。临床。翻译。医学12，e761（2022）。文章

PubMed

PubMed Central

公共医学中心

CAS

中科院

Google Scholar

谷歌学者

Wu, J. et al. Lysine methyltransferase SMYD2 inhibits antiviral innate immunity by promoting IRF3 dephosphorylation. Cell Death Dis. 14, 592 (2023).Article

Wu，J。等人。赖氨酸甲基转移酶SMYD2通过促进IRF3去磷酸化来抑制抗病毒先天免疫。细胞死亡Dis。14592（2023）。文章

PubMed

PubMed Central

公共医学中心

CAS

中科院

Google Scholar

谷歌学者

Wu, W. et al. SMYD2-mediated TRAF2 methylation promotes the NF-kappaB signaling pathways in inflammatory diseases. Clin. Transl. Med. 11, e591 (2021).Article

Wu，W。等人。SMYD2介导的TRAF2甲基化促进炎症性疾病中的NF-κB信号通路。临床。翻译。医学杂志11，e591（2021）。文章

PubMed

PubMed Central

公共医学中心

CAS

中科院

Google Scholar

谷歌学者

Liu, L. et al. Critical roles of SMYD2 lysine methyltransferase in mediating renal fibroblast activation and kidney fibrosis. FASEB J. 35, e21715 (2021).Article

Liu，L.等人。SMYD2赖氨酸甲基转移酶在介导肾成纤维细胞活化和肾纤维化中的关键作用。。文章

PubMed

CAS

中科院

Google Scholar

谷歌学者

Xu, W. et al. Ranunculus ternatus Thunb extract attenuates renal fibrosis of diabetic nephropathy via inhibiting SMYD2. Pharm. Biol. 60, 300–307 (2022).Article

Xu，W。等人。猫爪草提取物通过抑制SMYD2减轻糖尿病肾病的肾纤维化。药学生物学。60300–307（2022）。文章

PubMed

PubMed Central

公共医学中心

CAS

中科院

Google Scholar

谷歌学者

Hamamoto, R. et al. SMYD3 encodes a histone methyltransferase involved in the proliferation of cancer cells. Nat. Cell Biol. 6, 731–740 (2004).Article

。自然细胞生物学。6731-740（2004）。文章

PubMed

CAS

中科院

Google Scholar

谷歌学者

Yoshioka, Y. et al. SMYD3-mediated lysine methylation in the PH domain is critical for activation of AKT1. Oncotarget 7, 75023–75037 (2016).Article

Yoshioka，Y。等人。PH结构域中SMYD3介导的赖氨酸甲基化对于激活AKT1至关重要。Oncotarget 77523–75037（2016）。文章

PubMed

PubMed Central

公共医学中心

Google Scholar

谷歌学者

Yoshioka, Y. et al. Protein lysine methyltransferase SMYD3 is involved in tumorigenesis through regulation of HER2 homodimerization. Cancer Med. 6, 1665–1672 (2017).Article

Yoshioka，Y。等人。蛋白质赖氨酸甲基转移酶SMYD3通过调节HER2同源二聚化参与肿瘤发生。癌症医学61665-1672（2017）。文章

PubMed

PubMed Central

公共医学中心

CAS

中科院

Google Scholar

谷歌学者

Huang, Y. et al. SMYD3 promotes endometrial cancer through epigenetic regulation of LIG4/XRCC4/XLF complex in non-homologous end joining repair. Oncogenesis 13, 3 (2024).Article

Huang，Y。等人。SMYD3通过非同源末端连接修复中LIG4/XRCC4/XLF复合物的表观遗传调控促进子宫内膜癌。。文章

PubMed

PubMed Central

公共医学中心

CAS

中科院

Google Scholar

谷歌学者

Zeng, Y. et al. SMYD3 drives the proliferation in gastric cancer cells via reducing EMP1 expression in an H4K20me3-dependent manner. Cell Death Dis. 14, 386 (2023).Article

Zeng，Y。等人，SMYD3通过以H4K20me3依赖性方式降低EMP1表达来驱动胃癌细胞的增殖。细胞死亡Dis。14386（2023）。文章

PubMed

PubMed Central

公共医学中心

CAS

中科院

Google Scholar

谷歌学者

Yang, Y. et al. SMYD3 associates with the NuRD (MTA1/2) complex to regulate transcription and promote proliferation and invasiveness in hepatocellular carcinoma cells. BMC Biol. 20, 294 (2022).Article

Yang，Y。等人SMYD3与NuRD（MTA1/2）复合物结合，调节肝细胞癌细胞的转录并促进其增殖和侵袭。BMC生物。2024（2022）。文章

PubMed

PubMed Central

公共医学中心

CAS

中科院

Google Scholar

谷歌学者

Zhong, D., Zhan, Z., Zhang, J., Liu, Y. & He, Z. SMYD3 regulates the abnormal proliferation of non-small-cell lung cancer cells via the H3K4me3/ANO1 axis. J. Biosci. 47, 53 (2022).Li, J. et al. SMYD3 overexpression indicates poor prognosis and promotes cell proliferation, migration and invasion in non‑small cell lung cancer.

Zhong，D.，Zhan，Z.，Zhang，J.，Liu，Y。＆He，Z。SMYD3通过H3K4me3/ANO1轴调节非小细胞肺癌细胞的异常增殖。J、生物科学。47、53（2022年）。Li，J。等人。SMYD3过表达表明非小细胞肺癌预后不良，并促进细胞增殖，迁移和侵袭。

Int. J. Oncol. 57, 756–766 (2020).Article .

内景J.Oncol。57756-766（2020）。文章。

PubMed

PubMed Central

公共医学中心

CAS

中科院

Google Scholar

谷歌学者

Yue, F. R. et al. SMYD3 promotes colon adenocarcinoma (COAD) progression by mediating cell proliferation and apoptosis. Exp. Ther. Med. 20, 11 (2020).Article

Yue，F.R。等人。SMYD3通过介导细胞增殖和凋亡来促进结肠腺癌（COAD）的进展。实验温度。医学杂志20,11（2020）。文章

PubMed

PubMed Central

公共医学中心

CAS

中科院

Google Scholar

谷歌学者

Jiang, Y. et al. Overexpression of SMYD3 in ovarian cancer is associated with ovarian cancer proliferation and apoptosis via methylating H3K4 and H4K20. J. Cancer 10, 4072–4084 (2019).Article

Jiang，Y。等人。SMYD3在卵巢癌中的过表达通过甲基化H3K4和H4K20与卵巢癌增殖和凋亡相关。J、癌症104072-4084（2019）。文章

PubMed

PubMed Central

公共医学中心

CAS

中科院

Google Scholar

谷歌学者

Wang, G. et al. High expression of SMYD3 indicates poor survival outcome and promotes tumour progression through an IGF-1R/AKT/E2F-1 positive feedback loop in bladder cancer. Aging 12, 2030–2048 (2020).Article

Wang，G。等人。SMYD3的高表达表明膀胱癌的生存结果较差，并通过IGF-1R/AKT/E2F-1正反馈环促进肿瘤进展。12030-2048年（2020年）。文章

PubMed

PubMed Central

公共医学中心

CAS

中科院

Google Scholar

谷歌学者

Yang, Z. et al. Histone lysine methyltransferase SMYD3 promotes oral squamous cell carcinoma tumorigenesis via H3K4me3-mediated HMGA2 transcription. Clin. Epigenetics 15, 92 (2023).Article

Yang，Z。等人。组蛋白赖氨酸甲基转移酶SMYD3通过H3K4me3介导的HMGA2转录促进口腔鳞状细胞癌肿瘤发生。临床。表观遗传学15,92（2023）。文章

PubMed

PubMed Central

公共医学中心

CAS

中科院

Google Scholar

谷歌学者

Ikram, S. et al. The SMYD3-MAP3K2 signaling axis promotes tumor aggressiveness and metastasis in prostate cancer. Sci. Adv. 9, eadi5921 (2023).Article

Ikram，S。等人。SMYD3-MAP3K2信号轴促进前列腺癌的肿瘤侵袭性和转移。科学。Adv.9，eadi5921（2023年）。文章

PubMed

PubMed Central

公共医学中心

CAS

中科院

Google Scholar

谷歌学者

Lyu, T. et al. SMYD3 promotes implant metastasis of ovarian cancer via H3K4 trimethylation of integrin promoters. Int. J. Cancer 146, 1553–1567 (2020).Article

。《国际癌症杂志》1461553-1567（2020）。文章

PubMed

CAS

中科院

Google Scholar

谷歌学者

Zhang, L. et al. SMYD3 promotes epithelial ovarian cancer metastasis by downregulating p53 protein stability and promoting p53 ubiquitination. Carcinogenesis 40, 1492–1503 (2019).PubMed

Zhang，L。等人。SMYD3通过下调p53蛋白稳定性和促进p53泛素化来促进上皮性卵巢癌转移。致癌作用401492-1503（2019）。PubMed出版社

CAS

中科院

Google Scholar

谷歌学者

Wang, Y. et al. Amplification of SMYD3 promotes tumorigenicity and intrahepatic metastasis of hepatocellular carcinoma via upregulation of CDK2 and MMP2. Oncogene 38, 4948–4961 (2019).Article

Wang，Y。等人。SMYD3的扩增通过上调CDK2和MMP2促进肝细胞癌的致瘤性和肝内转移。癌基因384948-4961（2019）。文章

PubMed

CAS

中科院

Google Scholar

谷歌学者

Zhou, Z. et al. ANKHD1 is required for SMYD3 to promote tumor metastasis in hepatocellular carcinoma. J. Exp. Clin. Cancer Res. 38, 18 (2019).Article

Zhou，Z。等人。SMYD3需要ANKHD1来促进肝细胞癌的肿瘤转移。J、实验临床。癌症研究38,18（2019）。文章

PubMed

PubMed Central

公共医学中心

Google Scholar

谷歌学者

Liu, M. et al. LncRNA LTSCCAT promotes tongue squamous cell carcinoma metastasis via targeting the miR-103a-2-5p/SMYD3/TWIST1 axis. Cell Death Dis. 12, 144 (2021).Article

Liu，M。等人。LncRNA LTSCCAT通过靶向miR-103a-2-5p/SMYD3/TWIST1轴促进舌鳞状细胞癌转移。细胞死亡Dis。12144（2021）。文章

PubMed

PubMed Central

公共医学中心

Google Scholar

谷歌学者

Fenizia, C. et al. SMYD3 promotes the epithelial-mesenchymal transition in breast cancer. Nucleic Acids Res. 47, 1278–1293 (2019).Article

Fenizia，C。等人SMYD3促进乳腺癌的上皮-间质转化。核酸研究471278-1293（2019）。文章

PubMed

CAS

中科院

Google Scholar

谷歌学者

Jiang, Y., Zhou, T., Shi, Y., Feng, W. & Lyu, T. A SMYD3/ITGB6/TGFbeta1 positive feedback loop promotes the invasion and adhesion of ovarian cancer spheroids. Front. Oncol. 11, 690618 (2021).Article

Jiang，Y.，Zhou，T.，Shi，Y.，Feng，W。＆Lyu，T。A SMYD3/ITGB6/TGFbeta1正反馈环促进卵巢癌球体的侵袭和粘附。正面。Oncol公司。11690618（2021）。文章

PubMed

PubMed Central

公共医学中心

CAS

中科院

Google Scholar

谷歌学者

Wang, S. et al. SMYD3 induces sorafenib resistance by activating SMAD2/3-mediated epithelial-mesenchymal transition in hepatocellular carcinoma. iScience 26, 106994 (2023).Article

Wang，S。等人。SMYD3通过激活肝细胞癌中SMAD2/3介导的上皮-间质转化来诱导索拉非尼耐药。iScience 26106994（2023）。文章

PubMed

PubMed Central

公共医学中心

CAS

中科院

Google Scholar

谷歌学者

Lv, H. W. et al. SMYD3 confers cisplatin chemoresistance of NSCLC cells in an ANKHD1-dependent manner. Transl. Oncol. 14, 101075 (2021).Article

Lv，H。W。等人SMYD3以ANKHD1依赖性方式赋予NSCLC细胞顺铂化学抗性。翻译。Oncol公司。14101075（2021）。文章

PubMed

PubMed Central

公共医学中心

CAS

中科院

Google Scholar

谷歌学者

Wang, L. et al. SET and MYND domain-containing protein 3 inhibits tumor cell sensitivity to cisplatin. Oncol. Lett. 19, 3469–3476 (2020).PubMed

Wang，L。等人。含SET和MYND结构域的蛋白3抑制肿瘤细胞对顺铂的敏感性。Oncol公司。利特。193469-3476（2020）。PubMed出版社

PubMed Central

公共医学中心

CAS

中科院

Google Scholar

谷歌学者

Lukinovic, V. et al. SMYD3 impedes small cell lung cancer sensitivity to alkylation damage through RNF113A methylation-phosphorylation cross-talk. Cancer Discov. 12, 2158–2179 (2022).Article

Lukinovic，V。等人。SMYD3通过RNF113A甲基化磷酸化串扰阻止小细胞肺癌对烷基化损伤的敏感性。癌症发现。122158–2179（2022）。文章

PubMed

PubMed Central

公共医学中心

CAS

中科院

Google Scholar

谷歌学者

Nigam, N. et al. SMYD3 represses tumor-intrinsic interferon response in HPV-negative squamous cell carcinoma of the head and neck. Cell Rep. 42, 112823 (2023).Article

SMYD3抑制HPV阴性头颈部鳞状细胞癌中肿瘤内在的干扰素反应。细胞代表42112823（2023）。文章

PubMed

PubMed Central

公共医学中心

CAS

中科院

Google Scholar

谷歌学者

Gradl, S. et al. Discovery of the SMYD3 inhibitor BAY-6035 using thermal shift assay (TSA)-based high-throughput screening. SLAS Discov. 26, 947–960 (2021).Article

Gradl，S.等人。使用基于热位移测定（TSA）的高通量筛选发现SMYD3抑制剂BAY-6035。SLA Discov。26947-960（2021）。文章

PubMed

CAS

中科院

Google Scholar

谷歌学者

Parenti, M. D. et al. Discovery of the 4-aminopiperidine-based compound EM127 for the site-specific covalent inhibition of SMYD3. Eur. J. Med. Chem. 243, 114683 (2022).Article

Parenti，M.D.等人发现了基于4-氨基哌啶的化合物EM127，用于SMYD3的位点特异性共价抑制。。243114683（2022）。文章

PubMed

CAS

中科院

Google Scholar

谷歌学者

Huang, C. et al. Discovery of irreversible inhibitors targeting histone methyltransferase, SMYD3. ACS Med. Chem. Lett. 10, 978–984 (2019).Article

Huang，C.等。发现靶向组蛋白甲基转移酶SMYD3的不可逆抑制剂。ACS医学化学。利特。10978-984（2019）。文章

PubMed

PubMed Central

公共医学中心

CAS

中科院

Google Scholar

谷歌学者

Alshiraihi, I. M. et al. In silico/in vitro hit-to-lead methodology yields SMYD3 inhibitor that eliminates unrestrained proliferation of breast carcinoma cells. Int. J. Mol. Sci. 21 https://doi.org/10.3390/ijms21249549 (2020).Zhu, H. P. et al. Discovery of tetrahydrofuranyl spirooxindole-based SMYD3 inhibitors against gastric cancer via inducing lethal autophagy.

Alshiraihi，I.M.等人在计算机/体外命中引导方法中产生SMYD3抑制剂，其消除乳腺癌细胞的不受限制的增殖。Int.J.Mol.Sci。21https://doi.org/10.3390/ijms21249549（2020年）。Zhu，H.P.等。通过诱导致命的自噬发现基于四氢呋喃基螺环吲哚的SMYD3抑制剂抗胃癌。

Eur. J. Med. Chem. 246, 115009 (2023).Article .

欧洲医学化学杂志。246, 115009 (2023).第[UNK]条。

PubMed

CAS

中科院

Google Scholar

谷歌学者

Kontaki, H. et al. Targeting Smyd3 by next-generation antisense oligonucleotides suppresses liver tumor growth. iScience 24, 102473 (2021).Article

Kontaki，H。等人。通过下一代反义寡核苷酸靶向Smyd3抑制肝肿瘤生长。iScience 24102473（2021）。文章

PubMed

PubMed Central

公共医学中心

CAS

中科院

Google Scholar

谷歌学者

Lin, F. et al. STAT3-induced SMYD3 transcription enhances chronic lymphocytic leukemia cell growth in vitro and in vivo. Inflamm. Res. 68, 739–749 (2019).Article

Lin，F。等人。STAT3诱导的SMYD3转录在体外和体内增强慢性淋巴细胞白血病细胞的生长。发炎。第68739-749号决议（2019年）。文章

PubMed

CAS

中科院

Google Scholar

谷歌学者

Ma, W., Zhang, Y., Qi, Y. & Guo, S. STAT3 promotes chronic lymphocytic leukemia progression through upregulating SMYD3 expression. Arch. Med. Sci. 15, 1163–1175 (2019).Article

Ma，W.，Zhang，Y.，Qi，Y。＆Guo，S。STAT3通过上调SMYD3表达促进慢性淋巴细胞白血病进展。拱门。医学科学。151163-1175（2019）。文章

PubMed

CAS

中科院

Google Scholar

谷歌学者

Liu, C. et al. VHL-HIF-2alpha axis-induced SMYD3 upregulation drives renal cell carcinoma progression via direct trans-activation of EGFR. Oncogene 39, 4286–4298 (2020).Article

Liu，C。等人。VHL-HIF-2α轴诱导的SMYD3上调通过EGFR的直接反式激活驱动肾细胞癌进展。癌基因394286-4298（2020）。文章

PubMed

CAS

中科院

Google Scholar

谷歌学者

Lee, B. et al. The long non-coding RNA SPRIGHTLY and its binding partner PTBP1 regulate exon 5 skipping of SMYD3 transcripts in group 4 medulloblastomas. Neurooncol. Adv. 4, vdac120 (2022).PubMed

Lee，B。等人。长的非编码RNA SPRITLY及其结合伴侣PTBP1调节第4组髓母细胞瘤中SMYD3转录本的外显子5跳跃。神经肿瘤学。《vdac120》（2022）第4期。PubMed出版社

PubMed Central

公共医学中心

Google Scholar

谷歌学者

Codato, R. et al. The SMYD3 methyltransferase promotes myogenesis by activating the myogenin regulatory network. Sci. Rep. 9, 17298 (2019).Article

Codato，R。等人。SMYD3甲基转移酶通过激活肌生成素调节网络促进肌生成。Sci。代表917298（2019）。文章

PubMed

PubMed Central

公共医学中心

Google Scholar

谷歌学者

Sajic, T. et al. SMYD3: a new regulator of adipocyte precursor proliferation at the early steps of differentiation. Int. J. Obes. 48, 557–566 (2024).Della Bella, E. et al. Differential regulation of circRNA, miRNA, and piRNA during early osteogenic and chondrogenic differentiation of human mesenchymal stromal cells.

。内景J.Obes。48557-566（2024）。Della Bella，E。等人。人间充质基质细胞早期成骨和软骨分化过程中circRNA，miRNA和piRNA的差异调节。

Cells 9 https://doi.org/10.3390/cells9020398 (2020).Fittipaldi, R. et al. The lysine methylase SMYD3 modulates mesendodermal commitment during development. Cells 10 https://doi.org/10.3390/cells10051233 (2021).Han, S. et al. miR-1307-3p stimulates breast cancer development and progression by targeting SMYD4.

单元格9https://doi.org/10.3390/cells9020398（2020年）。赖氨酸甲基化酶SMYD3在发育过程中调节中胚层的承诺。单元格10https://doi.org/10.3390/cells10051233（2021年）。Han，S。等人。miR-1307-3p通过靶向SMYD4刺激乳腺癌的发展和进展。

J. Cancer 10, 441–448 (2019).Article .

J、癌症10441-448（2019）。文章。

PubMed

PubMed Central

公共医学中心

CAS

中科院

Google Scholar

谷歌学者

Zhou, Z. et al. SMYD4 monomethylates PRMT5 and forms a positive feedback loop to promote hepatocellular carcinoma progression. Cancer Sci. https://doi.org/10.1111/cas.16139 (2024).Chi, G. et al. SMYD5 acts as a potential biomarker for hepatocellular carcinoma. Exp. Cell Res. 414, 113076 (2022).Article .

。癌症科学。https://doi.org/10.1111/cas.16139（2024年）。Chi，G。等人。SMYD5作为肝细胞癌的潜在生物标志物。Exp.Cell Res.414113076（2022）。文章。

PubMed

CAS

中科院

Google Scholar

谷歌学者

Xiao, D. et al. The roles of SMYD4 in epigenetic regulation of cardiac development in zebrafish. PLoS Genet. 14, e1007578 (2018).Article

Xiao，D。等人。SMYD4在斑马鱼心脏发育表观遗传调控中的作用。PLoS Genet。14，e1007578（2018）。文章

PubMed

PubMed Central

公共医学中心

Google Scholar

谷歌学者

Kidder, B. L., Hu, G., Cui, K. & Zhao, K. SMYD5 regulates H4K20me3-marked heterochromatin to safeguard ES cell self-renewal and prevent spurious differentiation. Epigenetics Chromatin 10, 8 (2017).Article

Kidder，B.L.，Hu，G.，Cui，K。＆Zhao，K。SMYD5调节H4K20me3标记的异染色质，以保护ES细胞自我更新并防止虚假分化。。文章

PubMed

PubMed Central

公共医学中心

Google Scholar

谷歌学者

Rueda-Robles, A., Audano, M., Alvarez-Mercado, A. I. & Rubio-Tomas, T. Functions of SMYD proteins in biological processes: what do we know? An updated review. Arch. Biochem. Biophys. 712, 109040 (2021).Article

Rueda Robles，A.，Audano，M.，Alvarez-Mercado，A.I。和Rubio Tomas，T。SMYD蛋白在生物过程中的功能：我们知道什么？最新评论。拱门。生物化学。生物物理。712109040（2021）。文章

PubMed

CAS

中科院

Google Scholar

谷歌学者

Download referencesAcknowledgementsThis work was supported by a National Research Foundation of Korea (NRF) grant funded by the Ministry of Science, ICT and Future Planning (2018M3A9H3023077/2021M3A9H3016046, 2020R1C1C100743, 2022R1A2C1003118, RS-2023-00225239, RS-2024-00336620), the Korean Fund for Regenerative Medicine (KFRM) grant funded by the Korea government (the Ministry of Science and ICT, the Ministry of Health & Welfare, 21A0404L1) and the KRIBB Research Initiative Program.

下载参考文献致谢这项工作得到了韩国国家研究基金会（NRF）的资助，该基金由科学，信息通信技术和未来规划部资助（2018M3A9H3023077/2021M3A9H3016046、2020R1C100743、2022R1A2C1003118、RS-2023-00225239、RS-2024-00336620），韩国再生医学基金（KFRM）资助，由韩国政府（科学和信息通信技术部，卫生与福利部，21A0404L1）和克里布研究计划资助。

The funders had no role in the study design, data collection or analysis, decision to publish, or manuscript preparation.Author informationAuthors and AffiliationsKorea Research Institute of Bioscience and Biotechnology, Daejeon, 34141, Republic of KoreaTae-Su Han, Dae-Soo Kim, Mi-Young Son & Hyun-Soo ChoKorea University of Science and Technology, Daejeon, 34316, Republic of KoreaTae-Su Han, Dae-Soo Kim, Mi-Young Son & Hyun-Soo ChoDepartment of Biological Science, Sungkyunkwan University, Suwon, 16419, Republic of KoreaTae-Su Han, Mi-Young Son & Hyun-Soo ChoAuthorsTae-Su HanView author publicationsYou can also search for this author in.

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PubMed Google ScholarContributionsT.S. Han, D.S. Kim, M.Y. Son, and H.S. Cho: conception and design, writing and review of the manuscript, and study supervision.Corresponding authorsCorrespondence to

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Reprints and permissionsAbout this articleCite this articleHan, TS., Kim, DS., Son, MY. et al. SMYD family in cancer: epigenetic regulation and molecular mechanisms of cancer proliferation, metastasis, and drug resistance.

转载和许可本文引用本文Han，TS.，Kim，DS.，Son，MY。等人，《癌症中的SMYD家族：癌症增殖，转移和耐药性的表观遗传调控和分子机制》。

Exp Mol Med (2024). https://doi.org/10.1038/s12276-024-01326-8Download citationReceived: 02 April 2024Revised: 29 June 2024Accepted: 21 July 2024Published: 01 November 2024DOI: https://doi.org/10.1038/s12276-024-01326-8Share 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.

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