| Literature DB >> 26489607 |
Wen-Wen Chou1, Chung-Feng Huang1,2, Ming-Lun Yeh1,3, Yi-Shan Tsai1, Ming-Yen Hsieh1, Ching-I Huang1, Jee-Fu Huang1,2, Pei-Chien Tsai1, Edward Hsi4,3,5, Suh-Hang Hank Juo4,5, Wei-Lun Tsai6,7, Wan-Long Chuang1,2,8,9, Ming-Lung Yu1,2,8,9,10, Chia-Yen Dai11,12,13,14,15,16,17.
Abstract
MicroRNAs (miRNA) have been implicated in HCV infection. The present study analyzed the effects of let-7g on HCV infection in vitro, in clinical tissue and serum samples. Here, we show that the expression of let-7g in serum and liver tissue is significantly higher in patients with sustained virologic response (SVR). We show that interferon (IFN)/ribavirin (RBV) induces let-7g expression through p38/AP-1 signaling. Overexpression of let-7g reduced HCV gene or core protein level and inhibited the HCV viral load. The let-7g and IFN/RBV have additively inhibitory effect on HCV replication. These data implicate let-7g as a new therapeutic drug to additively cooperate with IFN/RBV to repress HCV replication. Key messages: let-7g expression is increased in serum and liver tissue of patients with SVR. Interferon/ribavirin induces let-7g expression through p38/AP-1 signaling. Overexpression of let-7g can repress HCV replication. Let-7g additively cooperates with interferon/ribavirin to repress HCV replication. Lin28B silencing can reverse let-7g expression and repress HCV replication.Entities:
Keywords: HCV; IFN; JFH; Let-7g; RBV
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Year: 2015 PMID： 26489607 DOI： 10.1007/s00109-015-1348-1
Source DB: PubMed Journal: J Mol Med (Berl) ISSN： 0946-2716 Impact factor: 4.599