| Literature DB >> 28069441 |
Hongpeng He1, Zhaoqiang Wei1, Fu Du1, Chao Meng1, Deliang Zheng1, Yongwei Lai1, Hailin Yao1, Hao Zhou1, Nan Wang1, Xue-Gang Luo1, Wenjian Ma1, Tong-Cun Zhang2.
Abstract
HOTAIR is a long non-coding RNA highly expressed in cancer tissues and is a negative prognostic factor, whereas the mechanism by which HOTAIR expression is upregulated in cancers remains elusive. In the present study, the regulation of HOTAIR transcription was investigated in breast cancer cells MCF7 and T47D. We found that, when the RhoC-ROCK signaling was disturbed by specific siRNAs or chemical inhibitors, the expression of HOTAIR would be down-regulated. Further, MRTF-A and SRF were found to affect HOTAIR expression. HOTAIR promoter activity was demonstrated to be regulated by the RhoC-MRTF-A-SRF signaling in a CArG-box-dependent manner. Moreover, MRTF-A was identified to physically interact with HOTAIR promoter, and RNA polymerase II association on HOTAIR promoter was enhanced by MRTF-A overexpression. Taken together, our results suggest that HOTAIR is regulated by the RhoC-MRTF-A-SRF signaling pathway in breast cancer cells.Entities:
Keywords: Breast cancer; HOTAIR; MRTF-A; Rho-signaling; Transcription
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Year: 2017 PMID： 28069441 DOI： 10.1016/j.cellsig.2017.01.003
Source DB: PubMed Journal: Cell Signal ISSN： 0898-6568 Impact factor: 4.315