Author/Authors :
Liu، نويسنده , , Chungang and Liu، نويسنده , , Limei and Shan، نويسنده , , Juanjuan and Shen، نويسنده , , Junjie and Xu، نويسنده , , Yanmin and Zhang، نويسنده , , Qianzhen and Yang، نويسنده , , Zhi and Wu، نويسنده , , Lin and Xia، نويسنده , , Feng and Bie، نويسنده , , Ping and Cui، نويسنده , , Youhong and Zhang، نويسنده , , Xia and Bian، نويسنده , , Xiuwu and Qian، نويسنده , , Cheng، نويسنده ,
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.
Keywords :
Cancer stem cells , Self-Renewal , HDAC3 , TSA , histone modification , HCC
