Splicing factor SF3a3 inhibits hepatitis C virus replication through PI3K-Akt pathway
10.3760/cma.j.issn.1003-9279.2016.01.008
- VernacularTitle:剪接因子 SF3 a3通过 PI3 K-Akt 信号传导通路调控丙型肝炎病毒的复制
- Author:
Xiaoqin DONG
1
;
Yaru LI
;
Jun CHENG
;
Hong ZHAO
Author Information
1. 100034,北京大学第一医院感染疾病科
- Keywords:
Splicing factor,SF3a;
Peglated Interferon-α,PEG-IFN-α;
Hepatitis C virus,HCV;
PI3K-Akt pathway
- From:
Chinese Journal of Experimental and Clinical Virology
2016;(1):30-33
- CountryChina
- Language:Chinese
-
Abstract:
Objective We sought to determine whether SF3a3 was capable of inhibiting HCV replication and to investigate the possible mechanisms.Methods Using the infectious HCV clones JFH1, we performed siRNA knockdown in Huh7.5.1 cells.First, we performed small interfering RNA (siRNA) to knock down SF3 gene expression.After 72 h incubation, Huh7.5.1 cells were infected with JFH1 for 24 h and then treated with 30IU/ml PEG-IFNα-2b for 48h.Members of SF3 family, HCV core and the key proteins of the IFN relative pathways were monitored by real time PCR and Western blot.Results SF3a3 mRNA level and protein expression were significantly decreased by SF3a3 specific siRNA compared with non-targeting siRNA, whose silencing effect was the best compared with other members of SF3a3 family;knockdown of SF3a3 protein expression by siRNA rescued HCV core expression, inhibited the role of interferon in anti-HCV infection under the same PEG-IFNα-2b pressure, and downregulated the phosphorylation of PI3K and Akt, as well as their total protein levels.Conclusions Silencing SF3a3 by specific siRNA could downregulate the expression of PI3K-Akt and p-PI3K/p-Akt proteins, which promoted the HCV replication.
