泛素连接酶
蛋白激酶B
生物
癌症研究
下调和上调
运动性
转移
调解人
PI3K/AKT/mTOR通路
转录因子
原癌基因蛋白质c-myc
癌症
泛素
癌变
信号转导
细胞生物学
基因
遗传学
作者
Xiaochen Liu,Jianfeng Cui,Li Gong,Fei Tian,Yajuan Shen,Lipeng Chen,Yong Wang,Yangyang Xia,Lei Liu,Yu‐Tao Xiang,Molin Wang,Guangyi Liu,Baichun Jiang,Changshun Shao,Yongxin Zou,Yaoqin Gong
出处
期刊:Oncogene
[Springer Nature]
日期:2020-03-03
卷期号:39 (17): 3588-3603
被引量:30
标识
DOI:10.1038/s41388-020-1236-1
摘要
CUL4B, which acts as a scaffold protein in CUL4B-RING ubiquitin ligase (CRL4B) complexes, participates in a variety of biological processes. Previous studies have shown that CUL4B is often overexpressed and exhibits oncogenic activities in a variety of solid tumors. However, the roles and the underlying mechanisms of CUL4B in bladder cancer (BC) were poorly understood. Here, we showed that CUL4B levels were overexpressed and positively correlated with the malignancy of BC, and CUL4B could confer BC cells increased motility, invasiveness, stemness, and chemoresistance. The PIK3CA/AKT pathway was identified as a critical downstream mediator of CUL4B-driven oncogenicity in BC cells. Furthermore, we demonstrated that CRL4B epigenetically repressed the transcription of miR-372/373, via catalyzing monoubiquitination of H2AK119 at the gene cluster encoding miR-372/373, leading to upregulation of PIK3CA and activation of AKT. Our findings thus establish a critical role for the CUL4B-miR-372/373-PIK3CA/AKT axis in the pathogenesis of BC and have important prognostic and therapeutic implications in BC.
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