The hepatitis B virus-associated estrogen receptor alpha （ERα） was regulated by microRNA-130a in HepG2.2.15 human hepatocellular carcinoma cells

The estrogen receptors （ERs） play important roles in hepatocarcinogenesis, which is always fostered by persistent hepatitis B virus （HBV） infection. Recent studies have linked microRNAs （miRNAs） to viral pathogenesis or oncogenesis. ERα could lead to cell cycle progression or inhibition of apoptosis...

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Published in生物化学与生物物理学报：英文版 Vol. 43; no. 8; pp. 640 - 646
Main Author Liping Tang Yong Pu Danny Ka-Ho Wong Tao Liu Hua Tang Tingxiu Xiang Man-Fung Yuen Guosheng Ren
Format Journal Article
LanguageEnglish
Published 2011
Subjects
HepG2细胞
microRNA
miRNA
乙型肝炎病毒
人肝癌细胞
增强型绿色荧光蛋白
雌激素受体α
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Summary:The estrogen receptors （ERs） play important roles in hepatocarcinogenesis, which is always fostered by persistent hepatitis B virus （HBV） infection. Recent studies have linked microRNAs （miRNAs） to viral pathogenesis or oncogenesis. ERα could lead to cell cycle progression or inhibition of apoptosis, while ERβ had opposite effects. Here we proposed that HBV affected ERs expression in viral oncogenesis, which might be triggered by miRNAs. The protein expression of ERα in HepG2.2.15 cells was much stronger than that in HepG2 cells, which was not consistent with its mRNA expression in these cells. MicroRNA-130a （miR-130a） was predicted to be a regulator of ERα by targeting its 3＇ untranslated region （3＇- UTR）. The enhanced green fluorescence protein （EGFP） reporter experiment confirmed the direct interaction of miR-130a and ERα. Moreover, ERα protein level was inversely correlated with the miR-130a level. Taken together, our studies supported that HBV infection might attenuate miR-130a expression and ERα was a direct target of miR-130a. Difference in miR-130a levels between HepG2 and HepG2.2.15 cells resulted in the difference in ERα expression, implying host-virus crosstalk in viral pathogenesis mediated by miRNAs.
Bibliography:estrogen receptor α; hepatitis B virus;microRNA; miR-130a
Liping Tang , Yong Pu, Danny Ka-Ho Wong, Tao Liu, Hua Tang, Tingxiu Xiang Man-Fung Yuen, and Guosheng Ren 1,IMolecular Oncology and Epigenetics Laboratory, the First Affiliated Hospital of Chongqing Medical University, Chongqing 400016, China 2Tianjin Life Science Research Center and Basic Medical School, Tianjin Medical University, Tianjin 300070, China 3Department of Medicine, Queen Mary Hospital, the University of Hong Kong, Hong Kong, China
The estrogen receptors （ERs） play important roles in hepatocarcinogenesis, which is always fostered by persistent hepatitis B virus （HBV） infection. Recent studies have linked microRNAs （miRNAs） to viral pathogenesis or oncogenesis. ERα could lead to cell cycle progression or inhibition of apoptosis, while ERβ had opposite effects. Here we proposed that HBV affected ERs expression in viral oncogenesis, which might be triggered by miRNAs. The protein expression of ERα in HepG2.2.15 cells was much stronger than that in HepG2 cells, which was not consistent with its mRNA expression in these cells. MicroRNA-130a （miR-130a） was predicted to be a regulator of ERα by targeting its 3＇ untranslated region （3＇- UTR）. The enhanced green fluorescence protein （EGFP） reporter experiment confirmed the direct interaction of miR-130a and ERα. Moreover, ERα protein level was inversely correlated with the miR-130a level. Taken together, our studies supported that HBV infection might attenuate miR-130a expression and ERα was a direct target of miR-130a. Difference in miR-130a levels between HepG2 and HepG2.2.15 cells resulted in the difference in ERα expression, implying host-virus crosstalk in viral pathogenesis mediated by miRNAs.
31-1940/Q
ISSN:1672-9145
1745-7270