| Literature DB >> 23879963 |
Chungang Liu1, Limei Liu, Juanjuan Shan, Junjie Shen, Yanmin Xu, Qianzhen Zhang, Zhi Yang, Lin Wu, Feng Xia, Ping Bie, Youhong Cui, Xia Zhang, Xiuwu Bian, Cheng Qian.
Abstract
Understanding molecular mechanisms in self-renewal of cancer stem cells (CSCs) is important for finding novel target in therapy of cancer. In this study, we explored potential effects of histone deacetylase (HDAC) on liver CSCs. Our data showed that HDAC inhibitors suppressed self-renewal and induced differentiation of liver CSCs. Furthermore, we demonstrated that HDAC3 was selectively expressed in liver CSCs and participated in self-renewal of liver CSCs via regulating expression of pluripotency factors. Overexpression of HDAC3 was associated with poor outcome of liver cancer. HDAC inhibitors could render liver CSCs sensitive to sorafenib. Taken together, our data suggest that HDAC3 plays a critical role in regulating self-renewal of liver CSCs.Entities:
Keywords: Cancer stem cells; HCC; HDAC3; Histone modification; Self-renewal; TSA
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Year: 2013 PMID： 23879963 DOI： 10.1016/j.canlet.2013.07.022
Source DB: PubMed Journal: Cancer Lett ISSN： 0304-3835 Impact factor: 8.679