Oncomir公司
基因敲除
小RNA
癌症研究
转移
六氯环己烷
癌变
肝细胞癌
生物
细胞生长
肿瘤进展
癌症
细胞培养
基因
遗传学
作者
Fang Ni,Hua Zhao,Huaqin Cui,Zhengsheng Wu,Li Chen,Zhongqian Hu,Chuang Guo,Yakun Liu,Zhuo Chen,Xinyi Wang,Danlei Chen,Haiming Wei,Siying Wang
出处
期刊:Cancer Letters
[Elsevier]
日期:2014-11-05
卷期号:356 (2): 809-818
被引量:69
标识
DOI:10.1016/j.canlet.2014.10.041
摘要
MicroRNAs are increasingly recognized as playing important roles in hepatocellular carcinoma (HCC) tumorigenesis. Here we identified an essential role for miR-362-5p in the regulation of HCC development. We found that miR-362-5p was significantly up-regulated in HCCs and associated with HCC progression. Inhibition of miR-362-5p in HCC cells dramatically decreased cell proliferation, clonogenicity, migration and invasion in vitro as well as tumor growth and metastasis in vivo. We subsequently identified that CYLD was a target gene of miR-362-5p. Furthermore, knockdown of CYLD expression partially counteracted the tumor suppressive effects of miR-362-5p inhibitors. Finally, we have shown that miR-362-5p acts through CYLD to activate the NF-κB signaling pathway, which contributes to HCC progression. Taken together, our findings indicate that miR-362-5p belongs to a new class of oncomiR that regulates HCC cell aggressiveness, thus providing new insight into the molecular mechanisms underlying HCC development. This study also suggests that miR-362-5p may serve as a novel therapeutic target for miRNA based HCC therapy.
科研通智能强力驱动
Strongly Powered by AbleSci AI