细胞周期蛋白
癌症研究
细胞周期蛋白D
细胞周期蛋白D1
周期素
细胞生物学
细胞生长
细胞周期
下调和上调
细胞周期蛋白B
细胞周期蛋白B1
细胞周期检查点
细胞周期蛋白A2
G1期
化学
生物
细胞
细胞周期蛋白依赖激酶1
基因
生物化学
作者
Qipeng Xie,Caiyi Chen,Haiying Li,Jiheng Xu,Lei Wu,Yu Yuan,Shuwei Ren,Hongyan Li,Xiaohui Hua,Yan Huang,Dapang Rao,Huxiang Zhang,Honglei Jin,Haishan Huang,Chuanshu Huang
标识
DOI:10.1016/j.ymthe.2019.03.006
摘要
Cyclin E2, a member of the cyclin family, is a key cell cycle-related protein. This protein plays essential roles in cancer progression, and, as such, an inhibitor of cyclin E2 has been approved to treat several types of cancers. Even so, mechanisms underlying how to regulate cyclin E2 expression in cancer remain largely unknown. In the current study, miR-3687 was upregulated in clinical bladder cancer (BC) tumor tissues, The Cancer Genome Atlas (TCGA) database, and human BC cell lines. Inhibition of miR-3687 expression significantly reduced human BC cell proliferation in vitro and tumor growth in vivo, which coincided with the induction of G0/G1 cell cycle arrest and downregulation of cyclin E2 protein expression. Interestingly, overexpression of cyclin E2 reversed the inhibition of BC proliferation induced by miR-3687. Mechanistic studies suggested that miR-3687 binds to the 3' UTR of foxp1 mRNA, downregulates FOXP1 protein expression, and in turn promotes the transcription of cyclin E2, thereby promoting the growth of BC cells. Collectively, the current study not only establishes a novel regulatory axis of miR-3687/FOXP1 regarding regulation of cyclin E2 expression in BC cells, but also provides strong suggestive evidence that miR-3687 and FOXP1 may be promising targets in therapeutic strategies for human BC.
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