泛素化和相关的细胞过程控制着人类细胞生物学的各个方面，这些过程的缺陷会导致多种疾病。近几十年来，我们对泛素化在淋巴癌中的病理作用以及针对修饰的泛素化系统的治疗策略的认识有了巨大的发展。在这里，我们回顾了由癌症相关 E2/E3 和去泛素化酶 (DUB) 的异常表达介导的信号机制改变，这些机制导致癌蛋白过度激活或肿瘤抑制因子经常联合下调。我们讨论了与几种不同的治疗干预措施有关的最新亮点，这些干预措施目前正在评估以有效阻断异常泛素-蛋白酶体途径，以及使用异双功能分子招募泛素化系统来降解或稳定非同源底物。本综述有助于理解淋巴癌中的泛素化异常和当前的靶向策略，并引发进一步的研究，以深入了解细胞泛素化与淋巴发病机制之间的联系，并改善相应的治疗干预措施。版权所有 © 2024。由 Elsevier B.V. 出版。

Ubiquitination and related cellular processes control a variety of aspects in human cell biology, and defects in these processes contribute to multiple illnesses. In recent decades, our knowledge about the pathological role of ubiquitination in lymphoid cancers and therapeutic strategies to target the modified ubiquitination system has evolved tremendously. Here we review the altered signalling mechanisms mediated by the aberrant expression of cancer-associated E2s/E3s and deubiquitinating enzymes (DUBs), which result in the hyperactivation of oncoproteins or the frequently allied downregulation of tumour suppressors. We discuss recent highlights pertaining to the several different therapeutic interventions which are currently being evaluated to effectively block abnormal ubiquitin-proteasome pathway and the use of heterobifunctional molecules which recruit the ubiquitination system to degrade or stabilise non-cognate substrates. This review aids in comprehension of ubiquitination aberrance in lymphoid cancers and current targeting strategies and elicits further investigations to deeply understand the link between cellular ubiquitination and lymphoid pathogenesis as well as to ameliorate corresponding treatment interventions.Copyright © 2024. Published by Elsevier B.V.