Research Papers:
Repression of miR1433p by HBx promotes hepatocellular carcinoma pathogenesis via BAG3
Bo Tang1, Guangying Qi1, Xingsi Liang1, Fang Tang1, Shengguang Yuan1, Zhenran Wang1, Shuiping Yu1, Xingyuan Jiao2 and Songqing He1
1Department of Hepatobiliary Surgery, Department of Pathology and Physiopathology, First Affiliated Hospital of Guangxi Medical University, Nanning, 530021, Guangxi, China
2Department of General Surgery, The First Affiliated Hospital, Sun Yat-Sen University, Guangzhou, 510080, Guangdong, China
Correspondence to:
Songqing He, email: [email protected]
Xingyuan Jiao, email: [email protected]
Keywords: HBX; microRNA-143; hepatocellular carcinoma; BAG3; apoptosis
Received: September 24, 2016 Accepted: August 28, 2017 Published:
ABSTRACT
Background: Hepatitis B virus (HBV) X protein (HBx) was correlated with progression of HBV infection associated hepatocellular carcinoma (HCC). The study was designed to understand the mechanism of miR-143-3p on progression in HBV induced HCC.
Method: Quantitative real-time Polymerase Chain Reaction (qRT-PCR) was performed to determinate the expression level of miR-143-3p and Bcl2-associated athanogene 3 (BAG3) in HBV (-) and HBV (+) human samples. Next, online database search and luciferase assay were conducted to evaluate the target genes of miR-143-3p. The relation between HBx and miR-143-3p or BAG3 was evaluated by using western-blot and qRT-PCR. The impact of miR-143-3p and HBx on cell proliferation and apoptosis was evaluated bby using MTT assay and flow cytometry assay.
Results: Comparing with human HBV (-) samples, the expression level of miR-143-3p significantly decreased in human HBV (+) samples. BAG3 is a direct target gene of miR-143-3p. The expression of BAG3 is significantly increased in the HBV (+) samples than that in the HBV (-) samples. HBx suppresses miR-143-3p and promotes BAG3 in HepG2 cells. HBx significantly promotes the proliferation and inhibits the apoptosis of HepG2 cells.
Conclusion: HBx inhibits miR-143-3p expression to promote liver cells proliferation and suppress apoptosis, which may explain its involvement in the tumorigenesis of HBV associated hepatocellular carcinoma.