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<p>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.</p>

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Role of the USP family in autophagy regulation and cancer progression

  • 期刊论文

  • 发表日期：

    2025年3月5日

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  • Congcong Liu,
  • Yalin Yuan,
  • Yuxin Zhan,
  • Mi Zou,
  • Linqian Wu,
  • Chunfang Zhang,
  • Bofan Chen,
  • Haimin Zeng,
  • Ruhui Yang,
  • Tianheng Hu,
  • Jie Peng,
  • Liang Hao

摘要

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.