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翻译抑制剂Pdcd4对耐药性的影响。

The Impact of Pdcd4, a Translation Inhibitor, on Drug Resistance.

作者信息

Wang Qing, Yang Hsin-Sheng

机构信息

Department of Toxicology and Cancer Biology, University of Kentucky, Lexington, KY 40536, USA.

Markey Cancer Center, University of Kentucky, Lexington, KY 40536, USA.

出版信息

Pharmaceuticals (Basel). 2024 Oct 19;17(10):1396. doi: 10.3390/ph17101396.

DOI:10.3390/ph17101396
PMID:39459035
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11510623/
Abstract

Programmed cell death 4 (Pdcd4) is a tumor suppressor, which has been demonstrated to efficiently suppress tumorigenesis. Biochemically, Pdcd4 binds with translation initiation factor 4A and represses protein translation. Beyond its role in tumor suppression, growing evidence suggests that Pdcd4 enhances the chemosensitivity of several anticancer drugs. To date, numerous translational targets of Pdcd4 have been identified. These targets govern important signal transduction pathways, and their attenuation may improve chemosensitivity or overcome drug resistance. This review will discuss the signal transduction pathways regulated by Pdcd4 and the potential mechanisms through which Pdcd4 enhances chemosensitivity or counteracts drug resistance.

摘要

程序性细胞死亡4(Pdcd4)是一种肿瘤抑制因子,已被证明能有效抑制肿瘤发生。在生物化学方面,Pdcd4与翻译起始因子4A结合并抑制蛋白质翻译。除了其在肿瘤抑制中的作用外,越来越多的证据表明Pdcd4可增强几种抗癌药物的化学敏感性。迄今为止,已鉴定出Pdcd4的众多翻译靶点。这些靶点控制着重要的信号转导途径,它们的减弱可能会提高化学敏感性或克服耐药性。本综述将讨论由Pdcd4调节的信号转导途径以及Pdcd4增强化学敏感性或对抗耐药性的潜在机制。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/faca/11510623/ab1e9a36b078/pharmaceuticals-17-01396-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/faca/11510623/9737e3309544/pharmaceuticals-17-01396-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/faca/11510623/d2af525976c5/pharmaceuticals-17-01396-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/faca/11510623/0aef8691e4e9/pharmaceuticals-17-01396-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/faca/11510623/4fcfc6ac588e/pharmaceuticals-17-01396-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/faca/11510623/ab1e9a36b078/pharmaceuticals-17-01396-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/faca/11510623/9737e3309544/pharmaceuticals-17-01396-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/faca/11510623/d2af525976c5/pharmaceuticals-17-01396-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/faca/11510623/0aef8691e4e9/pharmaceuticals-17-01396-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/faca/11510623/4fcfc6ac588e/pharmaceuticals-17-01396-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/faca/11510623/ab1e9a36b078/pharmaceuticals-17-01396-g005.jpg

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Human tumor suppressor protein Pdcd4 binds at the mRNA entry channel in the 40S small ribosomal subunit.人类肿瘤抑制蛋白Pdcd4结合于40S小核糖体亚基的mRNA进入通道。
Nat Commun. 2024 Aug 8;15(1):6633. doi: 10.1038/s41467-024-50672-8.
2
Human tumor suppressor PDCD4 directly interacts with ribosomes to repress translation.人类肿瘤抑制因子PDCD4直接与核糖体相互作用以抑制翻译。
Cell Res. 2024 Jul;34(7):522-525. doi: 10.1038/s41422-024-00962-z. Epub 2024 Apr 19.
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Genetics of in Cancer.癌症中的遗传学。 (你提供的原文不完整,推测是Genetics of [具体内容] in Cancer 这样的表述,但按照现有原文就是上述译文 )
Cancers (Basel). 2023 Aug 24;15(17):4236. doi: 10.3390/cancers15174236.
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The potential of activator protein 1 (AP-1) in cancer targeted therapy.AP-1 在癌症靶向治疗中的潜力。
Front Immunol. 2023 Jul 6;14:1224892. doi: 10.3389/fimmu.2023.1224892. eCollection 2023.
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Drugging IGF-1R in cancer: New insights and emerging opportunities.癌症中靶向胰岛素样生长因子-1受体(IGF-1R):新见解与新机遇
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Cells. 2022 Dec 15;11(24):4069. doi: 10.3390/cells11244069.
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