AbstractThe development of chemoresistance is a major challenge in the treatment of several types of cancers in clinical settings. Stemness and chemoresistance are the chief causes of poor clinical outcomes. In this context, we hypothesized that understanding the signaling pathways responsible for chemoresistance in cancers is crucial for the development of novel targeted therapies to overcome drug resistance.

摘要化疗耐药的发展是临床治疗几种癌症的主要挑战。干性和化学抗性是临床结果不佳的主要原因。在这种情况下，我们假设了解负责癌症化学抗性的信号传导途径对于开发克服耐药性的新型靶向疗法至关重要。

Among the aberrantly activated pathways, the PI3K-Akt/Wnt/β-catenin signaling pathway is clinically implicated in malignancies such as colorectal cancer (CRC) and glioblastoma multiforme (GBM). Aberrant dysregulation of phospholipase D (PLD) has been implicated in several malignancies, and oncogenic activation of this pathway facilitates tumor proliferation, stemness, and chemoresistance.

。磷脂酶D（PLD）的异常失调与几种恶性肿瘤有关，该途径的致癌激活促进肿瘤增殖，干性和化学抗性。

Crosstalk involving the PLD and Wnt/β-catenin pathways promotes the progression of CRC and GBM and reduces the sensitivity of cancer cells to standard therapies. Notably, both pathways are tightly regulated and connected at multiple levels by upstream and downstream effectors. Thus, gaining deeper insights into the interactions between these pathways would help researchers discover unique therapeutic targets for the management of drug-resistant cancers.

涉及PLD和Wnt/β-连环蛋白途径的串扰促进CRC和GBM的进展，并降低癌细胞对标准疗法的敏感性。值得注意的是，这两种途径都受到上游和下游效应子的严格调控并在多个层面上连接。因此，深入了解这些途径之间的相互作用将有助于研究人员发现治疗耐药癌症的独特治疗靶点。

Here, we review the molecular mechanisms by which PLD signaling stimulates stemness and chemoresistance in CRC and GBM. Thus, the current review aims to address the importance of PLD as a central player coordinating cross-talk between the PI3K/Akt and Wnt/β-catenin pathways and proposes the possibility of targeting these pathways to improve cancer therapy and overcome drug resistance..

在这里，我们回顾了PLD信号刺激CRC和GBM中干性和化学抗性的分子机制。因此，目前的综述旨在解决PLD作为协调PI3K/Akt和Wnt/β-连环蛋白之间串扰的中心参与者的重要性。途径，并提出了靶向这些途径以改善癌症治疗和克服耐药性的可能性。。

IntroductionOne of the current challenges in comprehensive cancer treatment is recurrence, which occurs after a period of remission, thereby contributing to treatment failure and disease progression. Colorectal cancer (CRC) continues to be one of the main causes of cancer-related deaths because patients exhibit disease progression and a poor prognosis related to resistance to current therapies.

引言目前综合癌症治疗面临的挑战之一是复发，复发发生在缓解期后，从而导致治疗失败和疾病进展。结直肠癌（CRC）仍然是癌症相关死亡的主要原因之一，因为患者表现出疾病进展和与对当前疗法的耐药性相关的不良预后。

Glioblastoma multiforme (GBM) is a devastating primary glial brain tumor; its overall prognosis remains dismal, and there is an unmet need for effective therapeutic strategies. Within the tumor bulk, there is a small population of neoplastic units, termed cancer stem cells (CSCs), and these cells play a vital role in CRC or GBM tumorigenesis, progression, maintenance, invasion and recurrence1,2,3,4.

多形性胶质母细胞瘤（GBM）是一种破坏性的原发性神经胶质脑肿瘤；其总体预后仍然不佳，对有效治疗策略的需求尚未得到满足。在肿瘤体积内，有一小部分肿瘤单位，称为癌症干细胞（CSCs），这些细胞在CRC或GBM肿瘤发生，进展，维持，侵袭和复发中起着至关重要的作用1,2,3,4。

Although the oncogenic roles of CSCs have not yet been completely elucidated, these slowly dividing cells are different from rapidly dividing tumor cells and are difficult to target using conventional therapies without harming adjacent nonneoplastic tissues5. Therefore, it is important to understand the mechanisms through which CSCs cause recurrence from several perspectives.

虽然CSCs的致癌作用尚未完全阐明，但这些缓慢分裂的细胞与快速分裂的肿瘤细胞不同，并且难以使用常规疗法靶向而不损害相邻的非肿瘤组织5。。

The CSC microenvironment stimulates signaling pathways such as the Wnt, Notch, and Hedgehog pathways to facilitate metastasis, invasion, and anoikis evasion6,7,8. Among the various signaling pathways involved in CSC-driven chemoresistance, aberrant activation of Wnt signaling appears to be essential for the maintenance of CSC populations, consequently altering patient clinical outcomes.

CSC微环境刺激信号通路，如Wnt，Notch和Hedgehog通路，以促进转移，侵袭和失巢凋亡6,7,8。在涉及CSC驱动的化学抗性的各种信号传导途径中，Wnt信号传导的异常激活似乎对于维持CSC群体至关重要，从而改变患者的临床结果。

Remarkably, 90% of CRC patients exhibit aberrant activation of the canonical Wnt/β-catenin signaling pathway9,10. Dysregulation of the Wnt/β-catenin pathway plays a fundamental role in the genesis and progression of several types .

值得注意的是，90%的CRC患者表现出经典Wnt/β-连环蛋白信号通路的异常激活9,10。Wnt/β-连环蛋白途径的失调在几种类型的发生和发展中起着重要作用。

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Download referencesAcknowledgementsThis work was supported by a National Research Foundation of Korea (NRF) grant funded by the Korean Government (MSIT) (No. 2023R1A2C100530811, RS-2023-00219297). Figures were created with BioRender.com.Author informationAuthor notesThese authors contributed equally: Seong Hun Lim, Hyesung Lee.Authors and AffiliationsDepartment of Pharmacy, Yonsei University, Incheon, 21983, Republic of KoreaSeong Hun Lim, Hyesung Lee, Hyun Ji Lee, Kuglae Kim, Junjeong Choi, Jung Min Han & Do Sik MinPOSTECH Biotech Center, Pohang University of Science and Technology, Pohang, 37673, Republic of KoreaJung Min HanYonsei Institute of Pharmaceutical Sciences, College of Pharmacy, Yonsei University, Incheon, 21983, Republic of KoreaDo Sik MinAuthorsSeong Hun LimView author publicationsYou can also search for this author in.

下载参考文献致谢这项工作得到了韩国政府（MSIT）资助的韩国国家研究基金会（NRF）资助（编号2023R1A2C100530811，RS-2023-00219297）的支持。数字是用BioRender.com.Author informationAuthor notes创建的。这些作者做出了同样的贡献：Seong Hun Lim，Hyesung Lee。作者和附属机构延世大学药学系，仁川，21983，韩国共和国延世大学药学院，洪林，李，李，金，崔俊贞，韩正民和多西明波斯特生物技术中心，浦项科技大学，浦项，37673，韩国共和国延世大学药学院，韩正民韩延世药物科学研究所，仁川，21983，韩国共和国作者出版物你也可以在中搜索这位作者。

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Reprints and permissionsAbout this articleCite this articleLim, S.H., Lee, H., Lee, H.J. et al. PLD1 is a key player in cancer stemness and chemoresistance: Therapeutic targeting of cross-talk between the PI3K/Akt and Wnt/β-catenin pathways.

转载和许可本文引用本文Lim，S.H.，Lee，H.，Lee，H.J.等人。PLD1是癌症干性和化学抗性的关键参与者：治疗靶向PI3K/Akt和Wnt/β-连环蛋白途径之间的串扰。

Exp Mol Med (2024). https://doi.org/10.1038/s12276-024-01260-9Download citationReceived: 29 December 2023Revised: 04 March 2024Accepted: 19 March 2024Published: 01 July 2024DOI: https://doi.org/10.1038/s12276-024-01260-9Share 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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