MicroRNA‐206 inhibits HCV proliferation through depressing ACC1 lipid synthesis signalling pathway

Abstract

Hepatitis C virus (HCV) infection was one of the main causes of hepatocellular carcinoma (HCC). Although direct antiviral drugs (DAA) were widely used to cure HCV patients and the recovery rate could reach 90%, avoiding HCV infection was still a challenge due to insufficiency of vaccine and animal model, anti-HCV drug resistance and incomplete diagnosis. Approximately 170 million persons were infected with HCV, 1 and 75% of them progressed to chronic HCV infection. 2 However, infectious progress of HCV patients and the production of HCC caused by HCV infection were not unclear. Thus, HCV infection and its pathogenesis needed to further study. Lipid metabolism participated in HCV infection and proliferation, and the hepatitis lipid pathway was suggested as a potential treatment target for HCV patients. 3 Moreover, HCV could remodel host lipid metabolism and increase itself replication. 4 The main function of microRNAs was to regulate the posttranscriptional level of its target message RNA (mRNA) by banding to mRNA 3′-untranslated region (3′-UTR). 5 MicroRNAs played critical roles in many signalling pathways, including lipid synthesis, immune system and neoplasia. microRNA-206 (miR-206) was firstly considered as muscle-specific microRNA, but researchers suggested that further comprehensive resource for miR-206 could be studied. 6 Then, Williams et al. identified that deficiency of miR-206 in