卵巢癌是一种致命疾病，由于诊断较晚和出现耐药性，限制了铂类治疗的疗效。耐药机制包括肿瘤内在因素和肿瘤微环境相关因素。去泛素酶 (DUB) 在卵巢癌中的作用开始显现。 DUB 是一大类酶，可从靶蛋白中去除泛素，并参与影响耐药性的过程，例如 DNA 损伤修复和细胞凋亡。此外，DUB 调节 T 细胞群的功能，有利于免疫抑制的微环境。三个 DUB 与蛋白酶体相关，而大多数则不然。在以前的 DUB 中，USP14 被认为可以调节 Bcl6 和 BACH1 等转录因子。此外，RPN11/PSMD14 会干扰包括上皮间质转化在内的各种过程，这也通过作用于 Snail 受到 USP1 等非蛋白酶体 DUB 的青睐。此外，USP8通过稳定HER家族受体可以赋予耐药性。总体而言，DUB 似乎是可药物化的，有几种抑制剂正在开发中。基于 DUB 的生物学作用，考虑到涉及不同治疗方法的联合策略，DUB 靶向似乎很有前景。在这里，我们总结了 DUB 在卵巢癌中的相关性，并提供了对该疾病治疗的未来挑战的见解。© 作者。

Ovarian cancer is a lethal disease due to late diagnosis and occurrence of drug resistance that limits the efficacy of platinum-based therapy. Drug resistance mechanisms include both tumor intrinsic and tumor microenvironment-related factors. A role for deubiquitinases (DUBs) is starting to emerge in ovarian cancer. DUBs are a large family of enzymes that remove ubiquitin from target proteins and participate in processes affecting drug resistance such as DNA damage repair and apoptosis. Besides, DUBs modulate the functions of T cell populations favoring an immune suppressed microenvironment. Three DUBs are proteasome-associated, whereas the large majority are not. Among the former DUBs, USP14 has been proposed to modulate transcription factors such as Bcl6 and BACH1. In addition, RPN11/PSMD14 interferes with various processes including epithelial mesenchymal transition, also favored by non-proteasomal DUBs such as USP1 by acting on Snail. Besides, USP8 by stabilizing HER family receptors can confer drug resistance. Overall, DUBs appear to be druggable, with several inhibitors under development. Based on DUBs biological role, DUBs targeting appears promising in view of combination strategies involving different therapeutic approaches. Here, we summarize the relevance of DUBs in ovarian carcinoma and provide insights into future challenges for the treatment of this disease.© The author(s).