Open Access

ARTICLE

HBx Downregulates miR-422a Expression via Activation of FOXG1/Q1/E1 in HepG2 Cells

Xiaofan Deng^1,2, Yamei Yang^2,3, Xianfeng Gan^2,3, Gang Wu^2,3,*

1 Organ Transplantation Center, Sichuan Provincial People’s Hospital, University of Electronic Science and Technology of China, Chengdu, 610072, China
2 Chinese Academy of Sciences Sichuan Translational Medicine Research Hospital, Chengdu, 610072, China
3 Department of Hepatobiliary Surgery, Sichuan Provincial People’s Hospital, University of Electronic Science and Technology of China, Chengdu, 610072, China

* Corresponding Author: Gang Wu. Email:

Oncologie 2021, 23(2), 251-258. https://doi.org/10.32604/Oncologie.2021.016900

Received 07 April 2021; Accepted 21 May 2021; Issue published 22 June 2021

Abstract

microRNA-422a (miR-422a) is downregulated in many hematopoietic tumors and solid tumors including hepatocellular carcinoma. We previously demonstrated that hepatitis B virus X protein (HBx) downregulated expression of miR-422a in HCC cell line HepG2 in vitro. However, we explore the mechanisms underlying this action. Forkhead box proteins (FOX) G1/Q1/E1 are known to negatively regulate miR-422a expression, and this prompted us to determine whether HBx suppresses miR-422a expression via activation of FOXG1/Q1/E1. The relationship between FOXG1/Q1/E1 and miR-422a in HepG2 cells stably expressing HBx was assessed with qRT-PCR. The correlation between HBx and FOXG1/Q1/E1 was determined with qRT-PCR and western blot in vitro. The cell cycle and CCK-8 assays were used to elucidate the consequence of miR-422a transfection in HepG2-hbx cells. FOXG1/Q1/E1 activated by HBx was found to be responsible, at least in part, for the downregulation of miR-422a in HepG2 cells. miR-422a transfection hampered the growth of HepG2-hbx cells by arresting cells in G1 phase. Both FOXG1/Q1/E1 and miR-422a may be suitable molecular targets for treatment of HBV-infected HCC.

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