國家衛生研究院 NHRI:Item 3990099045/2354

NHRI > Institute of Molecular and Genomic Medicine > King-Song Jeng(1997-2002) > Periodical Articles > Item 3990099045/2354

Please use this identifier to cite or link to this item: http://ir.nhri.org.tw/handle/3990099045/2354

Title:	Blocking of G1/S transition and cell death in the regenerating liver of Hepatitis B virus X protein transgenic mice
Authors:	Wu, BK;Li, CC;Chen, HJ;Chang, JL;Jeng, KS;Chou, CK;Hsu, MT;Tsai, TF
Contributors:	Division of Molecular and Genomic Medicine
Abstract:	The Hepatitis B Virus X (HBx) protein has been strongly implicated in the carcinogenesis of hepatocellular carcinoma (HCC). However, effects of the HBx protein on cell proliferation and cell death are controversial. This study investigates the effects of the HBx protein oil liver regeneration in two independent lines of HBx transgenic mice, which developed HCC at around 14 to 16 months of age. High mortality, lower liver mass restoration, and impaired liver regeneration were found in the HBx transgenic mice post-hepatectomy. The levels of alanine aminotransferase and alpha-fetoprotein detected post-hepatectomy increased significantly in the HBx transgenic livers, indicating that they were more susceptible to damage during the regenerative process. Prolonged activation of the immediate-early genes in the HBx transgenic livers Suggested that the HBx protein creates a strong effect by promoting the transition of the quiescent hepatocytes from G0 to G1 phase. However, impaired DNA synthesis and mitosis, as well as inhibited activation of G 1, S, and G2/M markers, were detected. These results indicated that HBx protein exerted strong growth arrest on hepatocytes and imbalanced cell-cycle progression resulting in the abnormal cell death; this was accompanied by severe fat accumulation and impaired glycogen storage in the HBx transgenic livers. In conclusion, this study provides the first physiological evidence that HBx protein blocks G1/S transition of the hepatocyte cell-cycle progression and causes both a failure of liver functionality and cell death in the regenerating liver of the HBx transgenic mice.
Keywords:	Biochemistry & Molecular Biology;Biophysics
Date:	2006-02-17
Relation:	Biochemical and Biophysical Research Communications. 2006 Feb;340(3):916-928.
Link to:	http://dx.doi.org/10.1016/j.bbrc.2005.12.089
JIF/Ranking 2023:	http://gateway.webofknowledge.com/gateway/Gateway.cgi?GWVersion=2&SrcAuth=NHRI&SrcApp=NHRI_IR&KeyISSN=0006-291X&DestApp=IC2JCR
Cited Times(WOS):	https://www.webofscience.com/wos/woscc/full-record/WOS:000235092000026
Cited Times(Scopus):	http://www.scopus.com/inward/record.url?partnerID=HzOxMe3b&scp=30144444237
Appears in Collections:	[King-Song Jeng(1997-2002)] Periodical Articles

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