TRAF4通过泛素化E2F1调控乳腺癌细胞凋亡  

TRAF4 regulates apoptosis by ubiquitinating E2F1 in breast cancer

作　　者：孙明芳 刁可心 王健[1] 米小轶[1] SUN Ming-fang;DIAO Ke-xin;WANG Jian;MI Xiao-yi(Department of Pathology,The First Affiliated Hospital of China Medical University,Shenyang 110001,China)

机构地区：[1]中国医科大学附属第一医院病理科,辽宁沈阳110001

出　　处：《解剖科学进展》2021年第3期305-308,共4页Progress of Anatomical Sciences

基　　金：国家自然科学基金面上项目(81572615)。

摘　　要：目的探讨肿瘤坏死因子受体相关因子4(TRAF4)是否通过E2F1转录因子(E2F1)调控乳腺癌细胞凋亡。方法流式细胞分析检测TRAF4对乳腺癌细胞凋亡的调控情况以及E2F1在其中的作用;Western blot检测TRAF4、精氨酸甲基转移酶5(PRMT5)和E2F1之间的调控关系;免疫荧光及免疫共沉淀检测TRAF4与E2F1的定位及相互作用。结果 TRAF4能够抑制乳腺癌细胞凋亡。TRAF4通过下调E2F1抑制乳腺癌细胞凋亡。TRAF4下调E2F1的作用不依赖PRMT5。TRAF4通过泛素化作用降解E2F1。结论在乳腺癌细胞中,TRAF4可以通过泛素化作用降解E2F1,并下调其表达水平,从而发挥其抑制凋亡的活性。Objective To investigate whether TNF receptor associated factor 4(TRAF4) regulated breast cancer cells apoptosis through E2 F transcription factor 1(E2F1). Methods Flow cytometric analysis detected the regulation of TRAF4 on apoptosis of breast cancer cells and the role of E2F1 in it. Western blot was used to detect the regulatory relationship among TRAF4, Protein arginine methyltransferase 5(PRMT5) and E2F1. Immunofluorescence and immunoprecipitation were used to detect the localization and interaction of TRAF4 and E2F1. Results TRAF4 can inhibit apoptosis of breast cancer cells. TRAF4 inhibited breast cancer cells apoptosis by down-regulating E2F1. The effect of TRAF4 down-regulating E2F1 did not depend on PRMT5. TRAF4 degraded E2F1 through ubiquitination. Conclusion In breast cancer cells, TRAF4 can degrade E2F1 through ubiquitination and down-regulate its protein expression, thereby inhibiting apoptosis.

关 键 词：乳腺癌 肿瘤坏死因子受体相关因子-4 泛素化 细胞凋亡 

分 类 号：R737.9[医药卫生—肿瘤]