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Title 

TGF-beta secreted from activated hepatic stellate cells may induce the transdifferentiation of hepatocytes into hepatocarcinoma in HBx-expressing livers

Authors 

M T HoY M KimDae Yeul YuD H LeeM ChoC Hyun

Publisher 

Korean Society for Applied Biological Chemisty

Issue Date 

2014

Citation 

Journal of Korean Society for Applied Biological Chemistry, vol. 57, no. 4, pp. 529-538

Keywords 

hepatic carcinogenesishepatic stellate cellshepatitis B virus X proteinhepatocyte transdifferentiationTGF-β

Abstract 

Hepatic stellate cells (HSCs) are the main extra cellular matrix-producing cells in the liver. Several reports have indicated that activated HSCs are involved in hepatic carcinogenesis by way of transforming growth factor β (TGF-β) secretion. This study aimed to investigate the effects of TGF-β, derived from HSCs activated by the chronic hepatitis B virus x protein (HBx), on the transdifferentiation of hepatocytes into hepatocarcinoma cells. Normal hepatocytes (the Chang liver cell line) were treated with a low concentration of TGF-β for 2 weeks, after which cell cycle- and cell signaling- related protein expression was analyzed. Lon-term treatment of TGF-β clearly induced the proliferation and the expression of cancer signaling proteins in the Chang cell line. TGF-β treatment also increased the expression of c-Jun N-terminal kinase (JNK) and c-Myc, indicating that induction of the JNK/pSmad3/c-Myc oncogenic signaling pathway is involved in hepatocyte transformation. Similar results were observed after culturing Chang cells with conditioned media derived from the activated LX-2 hepatic stellate cell line, suggesting that TGF-β paracrine effects are involved in the transformation of hepatocyte cells into hepatocarcinoma cells. Immunohistochemical results showed that the livers from HBx transgenic mice were composed of more activated HSCs and produced more TGF-β compared with those from normal mice. The TGF-β secreted from HBx-infected HSCs might induce transdifferentiation of hepatocytes into hepatocarcinoma, which is the fact that suggested a potential knowledge on liver cancer inhibition.

ISSN 

1738-2203

Link 

http://dx.doi.org/10.1007/s13765-014-4179-9

Appears in Collections

1. Journal Articles > Journal Articles

Registered Date

2017-04-19


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