COP1, an E3 ubiquitin ligase, has been demonstrated to play a vital role in the regulation of cell proliferation, apoptosis and DNA repair. Accumulated evidence has revealed that COP1 is involved in carcinogenesis via targeting its substrates, including p53, c-Jun, ETS, β-catenin, STAT3, MTA1, p27, 14-3-3σ, and C/EBPα, for ubiquitination and degradation. COP1 can play tumor suppressive and oncogenic roles in human malignancies, urging us to summarize the functions of COP1 in tumorigenesis. In this review, we describe the structure of COP1 and its known substrates. Moreover, we dissect the function of COP1 by physiological (mouse models), pathological (human tumor specimens) and biochemical (ubiquitin substrates) Evidence. Furthermore, we discuss COP1 as a potential therapeutic target for cancer therapy.

COP1 是一种 E3 泛素连接酶，已被证明在调节细胞增殖、细胞凋亡和 DNA 修复中起着至关重要的作用。越来越多的证据表明，COP1 通过靶向其底物参与致癌作用，包括 p53、c-Jun、ETS、β-catenin、STAT3、MTA1、p27、14-3-3σ 和 C/EBPα，用于泛素化和降解。COP1 可以在人类恶性肿瘤中发挥肿瘤抑制和致癌作用，促使我们总结 COP1 在肿瘤发生中的功能。在这篇综述中，我们描述了 COP1 及其已知底物的结构。此外，我们通过生理（小鼠模型）、病理（人类肿瘤标本）和生化（泛素底物）证据剖析 COP1 的功能。此外，我们讨论了 COP1 作为癌症治疗的潜在治疗靶点。