Sorafenib overcomes the chemoresistance in HBx-expressing hepatocellular carcinoma cells through down-regulation of HBx protein stability and suppresses HBV gene expression.

作者: Hye Young Kim , Hye Uk Jung , Seung Hee Yoo , Ki Soo Yoo , JaeHun Cheong

DOI: 10.1016/J.CANLET.2014.09.015

关键词:

摘要: Previous studies have revealed that HBx expression has anti-apoptotic effects, resulting in increased drug resistance HCC cells. Thus, we examined if sorafenib efficiently induces apoptosis HBx-overexpressing Noticeably, induced apoptosis, even HBx-expressing HepG2 cells, indicating the protein does not attenuate sorafenib-induced apoptosis. We next investigated modulates autophagy, allowing cells to overcome chemoresistance conferred by protein. Although autophagy plays a cytoprotective role against lethality, was effective irrespective of overexpression. exerts its cytotoxic effect via direct effects on Importantly, decreased stability through proteasome-dependent degradation pathway. Moreover, HBV gene and viral promoter activity. Taken together, apoptotic cell death downregulation protein, key factor anti-cancer observed HBV-induced HCC.

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