@Article{Oncologie.2021.016900,
AUTHOR = {Xiaofan Deng, Yamei Yang, Xianfeng Gan, Gang Wu},
TITLE = {HBx Downregulates miR-422a Expression via Activation of FOXG1/Q1/E1 in HepG2 Cells},
JOURNAL = {Oncologie},
VOLUME = {23},
YEAR = {2021},
NUMBER = {2},
PAGES = {251--258},
URL = {http://www.techscience.com/oncologie/v23n2/42960},
ISSN = {1765-2839},
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 <i>in vitro</i>. 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.},
DOI = {10.32604/Oncologie.2021.016900}
}