MicroRNA‐206 inhibits HCV proliferation through depressing ACC1 lipid synthesis signalling pathway. Issue 8 (28th May 2022)

• Record Type: Journal Article
• Authors: Zheng, Kexi; Xia, Tian; Liu, Ni; Xia, Xueshan; Song, Yuzhu; Zhang, A‐Mei
• Is Part Of: Journal of viral hepatitis. Volume 29:Issue 8(2022)
• Page Start: 654
• Page End: 660
• Publication Date: 2022-05-28
• Subjects: ACC1 -- inhibiting HCV proliferation -- lipid droplet -- lipogenesis -- microRNA‐206; Hepatitis, Viral -- Periodicals; Hepatitis, Viral, Animal; Hepatitis, Viral, Human; 616.3623
• DOI: 10.1111/jvh.13703
• Languages: English
• ISSNs: 1352-0504

Abstract

Abstract: MicroRNAs are considered to play important roles in cell biological and pathological progress. microRNA‐206 (miR‐206) was reported to participate in lipogenesis, and lipid droplets were necessary for the life cycle of HCV proliferation. Whether miR‐206 was associated with HCV proliferation and the potential mechanism are not clear. In this study, we firstly identified that miR‐206 could inhibit HCV proliferation at the RNA and protein level. Bioinformatical prediction of target genes binding to miR‐206 was performed to investigate whether inhibiting function was due to a lipogenesis pathway. Then, the acetyl‐CoA carboxylase 1 ( ACC1 ) gene was selected as target gene of miR‐206. The dual‐luciferase reporter assay results showed that luciferase significantly decreased in cells transfected with 3′‐UTR of the ACC1 gene and miR‐206. The RNA and protein levels of the ACC1 gene and its pathway genes were significantly lower in cells transfected with miR‐206 than in controls. Furthermore, the lipid droplet numbers also significantly decreased in cells transfected with miR‐206. In conclusion, miR‐206 could inhibit HCV proliferation through depressing ACC1 lipogenesis pathway and decreasing the lipid droplet numbers. miR‐206 might be used as anti‐HCV biochemical drug in the future.