USP8在乳腺癌中作用机制的研究进展

摘要

乳腺癌的临床治疗中,肿瘤复发和治疗耐药仍然构成主要挑战。泛素特异性蛋白酶8（USP8）是一种重要的去泛素化酶,近年来逐渐成为该领域的研究焦点。多项研究表明,USP8在乳腺癌组织中经常呈现异常表达,其主要通过阻遏雌激素受体α（ERα）和Notch信号通路等关键致癌蛋白的泛素化降解,促进肿瘤细胞的增殖、侵袭和转移,并参与内分泌治疗耐药的发生。此外,USP8还可调控肿瘤微环境,导致免疫抑制状态的形成,进而削弱免疫治疗的疗效。现有实验证据显示,针对USP8的小分子抑制剂具有显著的抗肿瘤活性。因此,进一步阐明USP8在乳腺癌中的分子机制,将有助于发现新型治疗靶点,尤其为克服耐药性的乳腺癌患者提供潜在的干预策略。

关键词

乳腺癌 / USP8 / 作用机制 / 研究进展

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