Interferon-α inhibits cell migration and invasion and induces the expression of antiviral proteins in Huh-7 cells transfected with hepatitis B virus X gene-expressing lentivirus

被引:1
|
作者
Yang, Qian [1 ]
Li, Xiao-Peng [1 ]
Zhong, Yuan-Bin [1 ]
Xiang, Tian-Xin [1 ]
Zhang, Lun-Li [1 ]
机构
[1] Nanchang Univ, Dept Infect Dis, Affiliated Hosp 1, 17 Yongwaizheng St, Nanchang 330006, Jiangxi, Peoples R China
关键词
hepatitis B virus X; interferon-alpha; Huh-7; antiviral protein; TRANSCRIPTIONAL ACTIVATION; LIVER-CANCER; THERAPY; HBX; PHOSPHORYLATION; REPLICATION; RECEPTOR; STAT3; PREVENTION; GUIDELINES;
D O I
10.3892/etm.2017.5288
中图分类号
R-3 [医学研究方法]; R3 [基础医学];
学科分类号
1001 ;
摘要
Hepatitis B virus (HBV) X protein (HBx) serves an important role in HBV infection and the development of HBV-related liver cancer. Interferon-alpha (IFN-alpha) is used to treat patients with HBV; however, the role of IFN-alpha in the development of HBV-related liver cancer remains unclear. The present study established a new HBV-related liver cancer model (Huh-7-HBx) by transfecting the hepatoma cell line Huh-7, with HBx-expressing lentivirus. Following IFN-alpha treatment, cell viability, migration and invasion, as well as the expression of antiviral proteins in Huh-7-HBx, were subsequently determined. The results demonstrated that HBx-expressing lentivirus had no significant effect on cell viability but promoted the migration and invasion of Huh-7 cells. The expression of the antiviral genes IFN alpha and beta receptor subunit 1 (IFNAR1), IFNAR2, IFN-stimulated gene factor 3, double-stranded RNA-activated protein kinase and ribonuclease L, was also increased. Following treatment of Huh-7-HBx cells with IFN-alpha, the expression of antiviral genes was increased at the level of transcription and translation, whereas cell migration and invasion was decreased. The present study suggests that IFN-alpha may attenuate the development of HBV-related liver cancer by reducing cell migration and invasion and promoting the expression of antiviral proteins.
引用
收藏
页码:5924 / 5930
页数:7
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