E3泛素连接酶在结直肠癌中的作用机制研究进展  

Recent advances in role of E3 ubiquitin ligases in colorectal cancer

作　　者：李芳 王珏 晏睿阳 李凯杨 沈慧 王丽[1] 张静[1] 张云清[2] LI Fang;WANG Jue;YAN Rui-yang;LI Kai-yang;SHEN Hui;WANG Li;ZHANG Jing;ZHANG Yun-qing(Medical School of Yan’an University,Yan’an Shaanxi 716000,China;Dept of Pathology,Affiliated Hospital of Yan′an University,Yan′an Shaanxi 716000,China)

机构地区：[1]延安大学医学院,陕西延安716000 [2]延安大学附属医院病理科,陕西延安716000

出　　处：《中国药理学通报》2023年第10期1811-1814,共4页Chinese Pharmacological Bulletin

基　　金：国家自然科学基金资助项目(No 82260530);陕西省自然科学基础研究计划项目(No 2022JQ-907);陕西省高校科协青年人才托举计划项目(No 20210309);2022年省级大学生创新创业训练计划项目(No S202210719089)。

摘　　要：结直肠癌(colorectal cancer,CRC)作为全球发病率和致死率最高的恶性肿瘤之一,其致病机制十分复杂,至今尚未完全阐明。泛素化在CRC的发生发展过程中扮演重要角色,其调控作用主要依赖于E3泛素连接酶泛素化修饰底物蛋白使之活性改变或发生泛素—蛋白酶体降解。该文就RING(really interesting new gene)型和HECT(homologous to E6AP C-terminus)型E3泛素连接酶在CRC细胞增殖、凋亡、迁移、侵袭及化疗敏感性中的作用机制及这两类E3泛素连接酶的靶向抑制剂相关研究进展作一综述,为CRC致病机制研究及其靶向治疗提供新的思路。Colorectal cancer(CRC)is one of the malignant tumors with the highest incidence and mortality in the world.The pathogenic mechanism of CRC has not been fully elucidated until now.Ubiquitination plays an important role in CRC development,and its effects mainly depend on E3 ubiquitin ligases,which could modify substrate proteins by ubiquitination,in turn altering their activity or mediating ubiquitin-proteasome degradation.Here research progress of the regulatory roles of RING(really interesting new gene)type and HECT(homologous to E6AP C-terminus)type E3 ubiquitin ligases in CRC cell proliferation,apoptosis,migration,invasion and chemotherapy sensitivity as well as targeted inhibitors of these E3 ligases are reviewed,providing new clues for the study of pathogenesis and targeted therapy of CRC.

关 键 词：E3泛素连接酶 结直肠癌 增殖 凋亡 迁移 侵袭 化疗敏感性 靶向抑制剂 

分 类 号：R329.25[医药卫生—人体解剖和组织胚胎学] R329.28[医药卫生—基础医学] R341.31R735.35R977.6