1. Differences in antiproliferative effect of STAT3 inhibition in HCC cells with versus without HBV expression.
- Author
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Hong, Yun, Zhou, Lin, Xie, Haiyang, Wang, Weilin, and Zheng, Shusen
- Subjects
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STAT proteins , *HEPATITIS B virus , *GENE expression in viruses , *LIVER cancer , *ETIOLOGY of diseases , *CELLULAR signal transduction - Abstract
Chronic infection with hepatitis B virus (HBV) plays an important role in the etiology of hepatocellular carcinoma (HCC). Signal transducer and activator of transcription 3 (STAT3) inactivation could inhibit the tumor growth of HCC. In this study, differential antiproliferative effect of STAT3 inhibition was observed with HBV-related HCC cells being more resistant than non-HBV-related HCC cells. Resistance of HBV-related HCC cells to STAT3 inhibition was positively correlated to the expression of HBV. Enhanced ERK activation after STAT3 blockade was detected in HBV-related HCC cells but not in non-HBV-related HCC cells. Combined ERK and STAT3 inhibition eliminates the discrepancy between the two types of HCC cells. Moderate reduced HBV expression was found after STAT3 inhibition. These findings disclose a discrepancy in cellular response to STAT3 inhibition between non-HBV-related and HBV-related HCC cells and underscore the complexity of antiproliferative effect of STAT3 inactivation in HBV-related HCC cells. [ABSTRACT FROM AUTHOR]
- Published
- 2015
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