| Literature DB >> 25449782 |
Fang Ni1, Hua Zhao2, Huaqin Cui2, Zhengsheng Wu3, Li Chen4, Zhongqian Hu2, Chuang Guo5, Yakun Liu2, Zhuo Chen2, Xinyi Wang2, Danlei Chen2, Haiming Wei6, Siying Wang7.
Abstract
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.Entities:
Keywords: CYLD; Hepatocellular carcinoma; Metastasis; miR-362-5p
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Year: 2014 PMID: 25449782 DOI: 10.1016/j.canlet.2014.10.041
Source DB: PubMed Journal: Cancer Lett ISSN: 0304-3835 Impact factor: 8.679