Role of the USP family in autophagy regulation and cancer progression

IF 8.1 2区 生物学 Q1 BIOCHEMISTRY & MOLECULAR BIOLOGY
Congcong Liu, Yalin Yuan, Yuxin Zhan, Mi Zou, Linqian Wu, Chunfang Zhang, Bofan Chen, Haimin Zeng, Ruhui Yang, Tianheng Hu, Jie Peng, Liang Hao
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引用次数: 0

Abstract

Autophagy is a vital pathway for recycling and degrading intracellular materials, closely linked to tumorigenesis and progression. The ubiquitin-specific protease (USP) family, as a critical group of deubiquitinating enzymes, plays a complex part in regulating autophagy, metabolism, immune responses, and tumor cells’ resistance to drugs. By modifying autophagy-associated proteins through deubiquitination, the USP family influences tumor cell proliferation, survival, and metabolism. Additionally, these enzymes are involved in modulating immune responses within the tumor microenvironment, thereby impacting tumor immune escape. Regarding drug resistance, the USP family enhances the tolerance of tumor cells to chemotherapeutic agents by promoting autophagy. Therefore, targeting USP family members and their regulated autophagy processes may offer new avenues for cancer therapy. This review examines the function of the USP family in tumor autophagy regulation and its implications for tumor progression. The goal of future studies should be to clarify the molecular mechanisms underlying USP-autophagy interactions and their specific roles in various tumor types to establish a theoretical framework for developing novel cancer therapeutic strategies.

USP家族在自噬调节和癌症进展中的作用。
自噬是细胞内物质循环和降解的重要途径,与肿瘤的发生和发展密切相关。泛素特异性蛋白酶(USP)家族是一类重要的去泛素化酶,在调节自噬、代谢、免疫反应和肿瘤细胞的耐药性等方面发挥着复杂的作用。USP家族通过去泛素化修饰自噬相关蛋白,影响肿瘤细胞的增殖、存活和代谢。此外,这些酶还参与调节肿瘤微环境中的免疫反应,从而影响肿瘤的免疫逃逸。在耐药性方面,USP家族通过促进自噬来增强肿瘤细胞对化疗药物的耐受性。因此,靶向USP家族成员及其调控的自噬过程可能为癌症治疗提供新的途径。本文综述了USP家族在肿瘤自噬调节中的功能及其对肿瘤进展的影响。未来研究的目标应该是阐明usp -自噬相互作用的分子机制及其在各种肿瘤类型中的具体作用,为开发新的癌症治疗策略建立理论框架。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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来源期刊
Apoptosis
Apoptosis 生物-生化与分子生物学
CiteScore
9.10
自引率
4.20%
发文量
85
审稿时长
1 months
期刊介绍: Apoptosis, a monthly international peer-reviewed journal, focuses on the rapid publication of innovative investigations into programmed cell death. The journal aims to stimulate research on the mechanisms and role of apoptosis in various human diseases, such as cancer, autoimmune disease, viral infection, AIDS, cardiovascular disease, neurodegenerative disorders, osteoporosis, and aging. The Editor-In-Chief acknowledges the importance of advancing clinical therapies for apoptosis-related diseases. Apoptosis considers Original Articles, Reviews, Short Communications, Letters to the Editor, and Book Reviews for publication.
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