HBx inhibits the growth of CCL13-HBX-stable cells via the GSK-3β/β-catenin cascade

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Title:	HBx inhibits the growth of CCL13-HBX-stable cells via the GSK-3β/β-catenin cascade
Authors:	Kuo, C.-Y.a, Wu, C.-C.b, Hsu, S.-L.c, Hwang, G.-Y.
Contributors:	Department of Life Science, Tunghai University
Keywords:	GSK-3β/β-catenin cascade;Hepatitis B virus X protein;Proliferation
Date:	2008
Issue Date:	2013-05-14T09:00:28Z (UTC)
Abstract:	Objective: The hepatitis B virus X protein (HBx) plays critical roles in cell survival via modulation of signaling pathways. In our previous studies, we reported that HBx inhibited the growth of CCL13-HBx-stable cells (Chang-HBx cells) in vitro and tumor formation in vivo in CCL13-HBx-cell-injected nude mice; however, this inhibition mechanism is unclear. Methods: To investigate the role of HBx in Wnt-3/β-catenin signaling pathways, we focused on the key molecules GSK-3β and β-catenin, and analyzed by Western blotting and immunofluorescence staining. Results: Results indicated that following HBx induction, GSK-3β activity was up-regulated, the expression and accumulation of β-catenin in the nucleus were decreased, and cell proliferation was suppressed. Inhibition of GSK-3β activity by pharmacological inhibitors rescued the expression and accumulation of β-catenin in the nucleus and facilitated cell proliferation and growth following HBx induction. The localization of β-catenin, which is involved in cell proliferation, and mediated by GSK-3β activation was also demonstrated. Conclusion: Our findings suggest that HBx negatively regulated proliferation of CCL13-HBx-stable cells via the GSK-3β/β-catenin cascade. Copyright ? 2008 S. Karger AG.
Relation:	Intervirology Volume 51, Issue 2, July 2008, Pages 130-136
Appears in Collections:	[生命科學系所] 期刊論文

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