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PINK1 介导的线粒体活性赋予前列腺癌细胞对奥拉帕利的耐药性。

PINK1-Mediated Mitochondrial Activity Confers Olaparib Resistance in Prostate Cancer Cells.

机构信息

Department of Urologic Surgery, University of California Davis, Davis, California.

Division of Hematology and Oncology, University of California Davis, Davis, California.

出版信息

Cancer Res Commun. 2024 Nov 1;4(11):2976-2985. doi: 10.1158/2767-9764.CRC-24-0339.

DOI:10.1158/2767-9764.CRC-24-0339
PMID:39440945
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11577557/
Abstract

Olaparib, a PARP inhibitor, is effective against various cancers, including prostate cancer. However, resistance to olaparib poses a significant challenge. This study uncovers that mitochondrial alterations and PINK1 gene overexpression contribute to this resistance in prostate cancer cells. Enhanced mitochondrial functionality and increased PINK1 expression in olaparib-resistant cells underscore the importance of targeting mitochondrial dynamics and PINK1 to develop more effective treatments for overcoming olaparib resistance in prostate cancer.

摘要

奥拉帕利（Olaparib）是一种 PARP 抑制剂，对包括前列腺癌在内的多种癌症有效。然而，奥拉帕利的耐药性是一个重大挑战。本研究揭示了线粒体改变和 PINK1 基因过表达导致前列腺癌细胞对奥拉帕利产生耐药性。在耐药细胞中，增强的线粒体功能和增加的 PINK1 表达强调了靶向线粒体动力学和 PINK1 的重要性，以开发更有效的治疗方法来克服前列腺癌中的奥拉帕利耐药性。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cff7/11577557/2c51ae4b2b2d/crc-24-0339_f6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cff7/11577557/cff998401881/crc-24-0339_f1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cff7/11577557/5d3b74ec8295/crc-24-0339_f2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cff7/11577557/c251ea939cc1/crc-24-0339_f3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cff7/11577557/89e85e07c26a/crc-24-0339_f4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cff7/11577557/af04fd570e6f/crc-24-0339_f5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cff7/11577557/2c51ae4b2b2d/crc-24-0339_f6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cff7/11577557/cff998401881/crc-24-0339_f1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cff7/11577557/5d3b74ec8295/crc-24-0339_f2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cff7/11577557/c251ea939cc1/crc-24-0339_f3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cff7/11577557/89e85e07c26a/crc-24-0339_f4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cff7/11577557/af04fd570e6f/crc-24-0339_f5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cff7/11577557/2c51ae4b2b2d/crc-24-0339_f6.jpg

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本文引用的文献

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IGFBP3 promotes resistance to Olaparib via modulating EGFR signaling in advanced prostate cancer.胰岛素样生长因子结合蛋白3（IGFBP3）通过调节晚期前列腺癌中的表皮生长因子受体（EGFR）信号传导来促进对奥拉帕尼的耐药性。
iScience. 2024 Jan 20;27(2):108984. doi: 10.1016/j.isci.2024.108984. eCollection 2024 Feb 16.
2
Abiraterone and Olaparib for Metastatic Castration-Resistant Prostate Cancer.阿比特龙联合奥拉帕利治疗转移性去势抵抗性前列腺癌
NEJM Evid. 2022 Sep;1(9):EVIDoa2200043. doi: 10.1056/EVIDoa2200043. Epub 2022 Jun 3.
3
Therapeutic Resistance Models and Treatment Sequencing in Advanced Prostate Cancer.
晚期前列腺癌的治疗耐药模型与治疗顺序
Cancers (Basel). 2023 Nov 3;15(21):5273. doi: 10.3390/cancers15215273.
4
PINK1-PTEN axis promotes metastasis and chemoresistance in ovarian cancer via non-canonical pathway.PINK1-PTEN 轴通过非经典途径促进卵巢癌的转移和化疗耐药。
J Exp Clin Cancer Res. 2023 Nov 9;42(1):295. doi: 10.1186/s13046-023-02823-w.
5
Current therapy and drug resistance in metastatic castration-resistant prostate cancer.转移性去势抵抗性前列腺癌的当前治疗与耐药性
Drug Resist Updat. 2023 May;68:100962. doi: 10.1016/j.drup.2023.100962. Epub 2023 Apr 14.
6
PINK1-Dependent Mitophagy Reduced Endothelial Hyperpermeability and Cell Migration Capacity Under Simulated Microgravity.在模拟微重力条件下，PINK1 依赖的线粒体自噬降低了内皮细胞的高通透性和细胞迁移能力。
Front Cell Dev Biol. 2022 Jul 7;10:896014. doi: 10.3389/fcell.2022.896014. eCollection 2022.
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Front Cell Dev Biol. 2022 Jul 8;10:954536. doi: 10.3389/fcell.2022.954536. eCollection 2022.
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