Downregulation of HBx Restrains Proliferation, Migration and Invasion of HepG2 Cells

Abstract

Background: Liver cancer is a frequent malignancy with high fatality. Hepatic B virus X protein (HBx) could promote theprogression of liver cancer. Meanwhile, aberrantly expressed XB130 was identified in liver cancer. However, relevant molecular mechanism is poorly studied. Our present study mainly investigated the mechanism of liver cancer.Methods: After microarray-based analyses in liver cancer tissues and the matched adjacent normal tissues, upregulated mRNA was screened out. Contents of HBx and XB130 in liver cancer tissues as well as cells HepG2 were examined by reverse transcription quantitative polymerase chain reaction (RT-qPCR) and Western blot analysis. Correlation between HBx and XB130 was analyzed in HepG2 cells, followed by verification by RIP assay. After gain- and loss-of-function experiments, cellular proliferation, invasion, migration and colony formation ability were assessed using CCK-8, Transwell, wound healing experiment and colony formation assay.Results: Both HBx and XB130 expression was elevated in liver cancer, which was correlated with poor survival rate of liver cancer patients. Moreover, HBx and XB130 were positively correlated in HepG2 cells. RIP assay verified that HBx could bind to XB130. Loss of HBx hindered proliferation, and migration/invasion of HepG2 cells but promoted apoptosis, which was partially reversed by overexpressed XB130.Conclusion: The conclusion reached from the study offered an understanding of the role of HBx/XB130 played in liver cancer. Our study first reported the regulatory relation between HBx and XB130, which may be valuable to discover therapeutic targets for liver cancer treatment.