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自噬:揭示癌症中的机制及多方面作用

Autophagy: Shedding Light on the Mechanisms and Multifaceted Roles in Cancers.

作者信息

You Hongmei, Wang Ling, Meng Hongwu, Li Jun, Fang Guoying

机构信息

Department of Pharmacy, Hangzhou Women's Hospital, Hangzhou 310000, China.

Department of Pharmacy, Shangyu People's Hospital of Shaoxing, Shaoxing 312000, China.

出版信息

Biomolecules. 2025 Jun 22;15(7):915. doi: 10.3390/biom15070915.


DOI:10.3390/biom15070915
PMID:40723786
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC12292191/
Abstract

Autophagy, an evolutionarily conserved self-degradation catabolic mechanism, is crucial for recycling breakdown products and degrading intracellular components such as cytoplasmic organelles, macromolecules, and proteins in eukaryotes. The process, which can be selective or non-selective, involves the removal of specific ribosomes, protein aggregates, and organelles. Although the specific mechanisms governing various aspects of selective autophagy have not been fully understood, numerous studies have revealed that the dysregulation of autophagy-related genes significantly influences cellular homeostasis and contributes to a wide range of human diseases, particularly cancers, neurodegenerative disorders and inflammatory diseases. Notably, accumulating evidence highlights the complex, dual role of autophagy in cancer development. Thus, this review systematically summarizes the molecular mechanisms of autophagy and presents the latest research on its involvement in both pro- and anti-tumor progression. Furthermore, we discuss the role of autophagy in cancer development and summarize advancement in tumor therapies targeting autophagy.

摘要

自噬是一种进化上保守的自我降解分解代谢机制,对于真核生物中分解产物的循环利用以及细胞质细胞器、大分子和蛋白质等细胞内成分的降解至关重要。该过程可以是选择性的或非选择性的,涉及特定核糖体、蛋白质聚集体和细胞器的清除。尽管尚未完全了解调控选择性自噬各个方面的具体机制,但大量研究表明,自噬相关基因的失调会显著影响细胞稳态,并导致多种人类疾病,尤其是癌症、神经退行性疾病和炎症性疾病。值得注意的是,越来越多的证据凸显了自噬在癌症发展中的复杂双重作用。因此,本综述系统地总结了自噬的分子机制,并介绍了其在肿瘤发生发展的促进和抑制作用方面的最新研究。此外,我们讨论了自噬在癌症发展中的作用,并总结了针对自噬的肿瘤治疗进展。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bbf1/12292191/82406c38a2a7/biomolecules-15-00915-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bbf1/12292191/99010c748706/biomolecules-15-00915-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bbf1/12292191/439188a7d63a/biomolecules-15-00915-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bbf1/12292191/82406c38a2a7/biomolecules-15-00915-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bbf1/12292191/99010c748706/biomolecules-15-00915-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bbf1/12292191/439188a7d63a/biomolecules-15-00915-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bbf1/12292191/82406c38a2a7/biomolecules-15-00915-g003.jpg

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本文引用的文献

[1]
Self-propelled smart nanomotors for enhanced mild photothermal therapy of tumors through autophagy modulation.

Acta Biomater. 2025-7-1

[2]
Overexpression of c-Myc triggers p62 aggregation-mediated mitochondrial mitophagy in cabozantinib resistance of hepatocellular carcinoma.

Mol Med. 2025-5-27

[3]
GPX4-AUTAC induces ferroptosis in breast cancer by promoting the selective autophagic degradation of GPX4 mediated by TRAF6-p62.

Cell Death Differ. 2025-5-20

[4]
Chemically engineered antibodies for autophagy-based receptor degradation.

Nat Chem Biol. 2025-1-9

[5]
Targeting autophagy plus high-dose CDK4/6 inhibitors in advanced HR+HER2- breast cancer: A phase 1b/2 trial.

Med. 2025-5-9

[6]
Cancer immunotherapeutic challenges from autophagy-immune checkpoint reciprocal regulation.

Trends Cancer. 2025-2

[7]
Autophagy in cancer development, immune evasion, and drug resistance.

Drug Resist Updat. 2025-1

[8]
CircSEC24B activates autophagy and induces chemoresistance of colorectal cancer via OTUB1-mediated deubiquitination of SRPX2.

Cell Death Dis. 2024-9-27

[9]
Enhancing antitumor efficacy of CLDN18.2-directed antibody-drug conjugates through autophagy inhibition in gastric cancer.

Cell Death Discov. 2024-9-3

[10]
Age- and disease-related autophagy impairment in Huntington disease: New insights from direct neuronal reprogramming.

Aging Cell. 2024-8

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