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The hepatitis B virus X protein induced fibrosis in Huh7 cells
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 Title & Authors
The hepatitis B virus X protein induced fibrosis in Huh7 cells
Son, Moa; Park, Sanggyu; Cho, Moonjae;
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 Abstract
Hepatitis B virus infection can cause hepatic fibrosis leading to cirrhosis and hepatocellular carcinoma. However the mechanism remains poorly understood. In this study, we found that Hepatitis B virus X-protein (HBx) increases vimentin, fibronectin, slug, snail and NOX4 expression. Because NOX4-mediated reactive oxygen species can increase slug and snail, which can induce fibrosis, HBx may be a key regulator of hepatic fibrosis development via NOX4 induction.
 Keywords
hepatic fibrosis;hepatitis B virus X protein;NADPH oxidase;
 Language
Korean
 Cited by
 References
1.
Albanis E and Friedman SL (2001) Hepatic fibrosis. Pathogenesis and principles of therapy. Clin Liver Dis 5, 315,34, v-vi.

2.
Boudreau HE, Casterline BW, Rada B, Korzeniowska A, and Leto TL (2012) Nox4 involvement in TGF-beta and SMAD3-driven induction of the epithelial-to-mesenchymal transition and migration of breast epithelial cells. Free Radic Biol Med 53, 1489-99. crossref(new window)

3.
De Minicis S and Brenner DA (2007) NOX in liver fibrosis. Arch Biochem Biophys 462, 266-72. crossref(new window)

4.
Guo GH, Tan DM, Zhu PA, and Liu F (2009) Hepatitis B virus X protein promotes proliferation and upregulates TGF-beta1 and CTGF in human hepatic stellate cell line, LX-2. Hepatobiliary Pancreat Dis Int 8, 59-64.

5.
Ha HL and Yu DY (2010) HBx-induced reactive oxygen species activates hepatocellular carcinogenesis via dysregulation of PTEN/Akt pathway. World J Gastroenterol 16, 4932-7. crossref(new window)

6.
Hiraga R, Kato M, Miyagawa S, and Kamata T (2013) Nox4-derived ROS signaling contributes to TGF-beta-induced epithelial-mesenchymal transition in pancreatic cancer cells. Anticancer Res 33, 4431-8.

7.
Jiang F, Liu GS, Dusting GJ, and Chan EC (2014) NADPH oxidasedependent redox signaling in TGF-beta-mediated fibrotic responses. Redox Biol 2, 267-72. crossref(new window)

8.
Kim YM and Cho M (2014) Activation of NADPH oxidase subunit NCF4 induces ROS-mediated EMT signaling in HeLa cells. Cell Signal 26, 784-96. crossref(new window)

9.
Nam HJ, Park YY, Yoon G, Cho H, and Lee JH (2010) Co-treatment with hepatocyte growth factor and TGF-beta1 enhances migration of HaCaT cells through NADPH oxidase-dependent ROS generation. Exp Mol Med 42, 270-9. crossref(new window)

10.
Novo E and Parola M (2008) Redox mechanisms in hepatic chronic wound healing and fibrogenesis. Fibrogenesis & Tissue Repair 1, 5. crossref(new window)

11.
Park SM, Kim SM, and Han JH (2010) The role of epithelial-mesenchymal transition in the gastroenterology. Korean J Gastroenterol 56, 69-77. crossref(new window)

12.
Serrander L, Cartier L, Bedard K, Banfi B, Lardy B, Plastre O et al. (2007) NOX4 activity is determined by mRNA levels and reveals a unique pattern of ROS generation. Biochem J 406, 105-14. crossref(new window)

13.
Shepard CW, Simard EP, Finelli L, Fiore AE, and Bell BP (2006) Hepatitis B virus infection: epidemiology and vaccination. Epidemiol Rev 28, 112-25. crossref(new window)

14.
Vassiliadis E, Oliveira CP, Alvares-da-Silva MR, Zhang C, Carrilho FJ, Stefano JT et al. (2012) Circulating levels of citrullinated and MMPdegraded vimentin (VICM) in liver fibrosis related pathology. Am J Transl Res 4, 403-14.

15.
Virtakoivu R, Mai A, Mattila E, De Franceschi N, Imanishi SY, Corthals G et al. (2015) Vimentin-ERK Signaling Uncouples Slug Gene Regulatory Function. Cancer Res 75, 2349-62. crossref(new window)

16.
Yang C, Song B, and Cho M (2012) A Natural Mutation of the Hepatitis B Virus X Gene Affects Cell Cycle Progression and Apoptosis in Huh7 Cells. J Korean Soc Appl Biol Chem. 55, 229-36. crossref(new window)

17.
Zhang M, Wang F, Chong Y, Tai Q, Zhao Q, Zheng Y et al. (2014) Liver myofibroblasts from hepatitis B related liver failure patients may regulate natural killer cell function via PGE2. J Transl Med 12, 308,014-0308-9.