Abstract A2-21: Cancer malignancy induced by C-terminal truncated HBx in Huh-7 Hepatocellular carcinoma cells

Abstract

Abstract Hepatitis B virus-encoded HBx is well known causative factor for the Hepatocellular carcinoma (HCC). HBx interferes with several signaling pathways that are associated with cell proliferation and apoptosis. HBx c-terminal region has been known to play important roles in HBV associated HCC. HBx C-terminal mutant was known to show increased proliferation and invasiveness. In this study, we investigated a molecular mechanism of cancer malignancy induced by C-terminal truncated HBx. Huh-7 Hepatocellular carcinoma cells stably transfected with C-terminal truncated HBx showed higher migrative and invasive phenotype. In addition, the cells were more resistant to doxorubicin compared to cells transfected with full-length HBx. We also observed a higher efflux activity in the cells transfected with C-terminal truncated HBx due to the increased expression of ABCB1. These results suggest that C-terminal truncated HBx up-regulate ABCB1 expression which results in the enhanced efflux of drug. Therefore cancer cells containing C-terminal truncated HBx acquire drug resistancy, and show more malignant phenotypes. Citation Format: Myeong-Eun Je Gal, Eui-Yeun Yi, Seung-Youn Jung, Yung-Jin Kim. Cancer malignancy induced by C-terminal truncated HBx in Huh-7 Hepatocellular carcinoma cells. [abstract]. In: Proceedings of the AACR Special Conference on Translation of the Cancer Genome; Feb 7-9, 2015; San Francisco, CA. Philadelphia (PA): AACR; Cancer Res 2015;75(22 Suppl 1):Abstract nr A2-21.