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NS5ATP9 Contributes to Inhibition of Cell Proliferation by Hepatitis C Virus (HCV) Nonstructural Protein 5A (NS5A) via MEK/Extracellular Signal Regulated Kinase (ERK) Pathway
Authors:Qi Wang  Yongsheng Wang  Yue Li  Xuesong Gao  Shunai Liu  Jun Cheng
Affiliation:1.Institute of Infectious Diseases, Beijing Ditan Hospital, Capital Medical University, Beijing 100015, China; E-Mails: (Q.W.); (Y.W.); (X.G.); (S.L.);2.Beijing Key Laboratory of Emerging Infectious Diseases, Beijing 100015, China;3.Institute of Materia Medica, Chinese Academy of Medical Sciences & Perking Union Medical College, Beijing 100050, China;4.Beijing Center for Physical and Chemical Analysis, Beijing 100094, China; E-Mail:
Abstract:Hepatitis C virus (HCV) nonstructural protein 5A (NS5A) is a remarkable protein as it clearly plays multiple roles in mediating viral replication, host-cell interactions and viral pathogenesis. However, on the impact of cell growth, there have been different study results. NS5ATP9, also known as KIAA0101, p15PAF, L5, and OEACT-1, was first identified as a proliferating cell nuclear antigen-binding protein. Earlier studies have shown that NS5ATP9 might play an important role in HCV infection. The aim of this study is to investigate the function of NS5ATP9 on hepatocellular carcinoma (HCC) cell lines proliferation under HCV NS5A expression. The results showed that overexpression of NS5ATP9 inhibited the proliferation of Bel7402 cells, whereas knockdown of NS5ATP9 by interfering RNA promoted the growth of HepG2 cells. Under HCV NS5A expression, RNA interference (RNAi) targeting of NS5ATP9 could reverse the inhibition of HepG2 cell proliferation, suggesting that NS5ATP9 might be an anti-proliferation gene that plays an important role in the suppression of cell growth mediated by HCV NS5A via MEK/ERK signaling pathway. These findings might provide new insights into HCV NS5A and NS5ATP9.
Keywords:HCV   NS5A   NS5ATP9   cell proliferation   MEK/ERK
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