Please use this identifier to cite or link to this item: http://hdl.handle.net/10397/43933
Title: Sirtuin 3 inhibits hepatocellular carcinoma growth through the glycogen synthase kinase-3β/BCL2-associated X protein-dependent apoptotic pathway
Authors: Song, CL
Tang, H
Ran, LK
Ko, BCB 
Zhang, ZZ
Chen, X
Ren, JH
Tao, NN
Li, WY
Huang, AL
Chen, J
Issue Date: 2016
Publisher: Nature Publishing Group
Source: Oncogene, 2016, v. 35, no. 5, p. 631-641 How to cite?
Journal: Oncogene 
Abstract: SIRT3 is a class III histone deacetylase that has been implicated in a variety of cancers. The role of SIRT3 in hepatocellular carcinoma (HCC) remains elusive. In this study, we found that SIRT3 expression was frequently repressed in HCC and its downregulation was closely associated with tumor grade and size. Ectopic expression of SIRT3 inhibited cell growth and induced apoptosis in HCC cells, whereas depletion of SIRT3 in immortalized hepatocyte promoted cell growth and decreased epirubicin-induced apoptosis. Mechanistic studies revealed that SIRT3 deacetylated and activated glycogen synthase kinase-3β (GSK-3β), which subsequently induced expression and mitochondrial translocation of the pro-apoptotic protein BCL2-associated X protein (Bax) to promote apoptosis. GSK-3β inhibitor or gene silencing of BAX reversed SIRT3-induced growth inhibition and apoptosis. Furthermore, SIRT3 overexpression also suppressed tumor growth in vivo. Together, this study reveals a role of SIRT3/GSK-3β/Bax signaling pathway in the suppression of HCC growth, and also suggests that targeting this pathway may represent a potential therapeutic approach for HCC treatment.
URI: http://hdl.handle.net/10397/43933
ISSN: 0950-9232
DOI: 10.1038/onc.2015.121
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