在人乳腺癌细胞中，HOTAIR的转录受RhoC-MRTF-A-SRF信号通路调控。
Transcription of HOTAIR is regulated by RhoC-MRTF-A-SRF signaling pathway in human breast cancer cells.
作者信息
He Hongpeng, Wei Zhaoqiang, Du Fu, Meng Chao, Zheng Deliang, Lai Yongwei, Yao Hailin, Zhou Hao, Wang Nan, Luo Xue-Gang, Ma Wenjian, Zhang Tong-Cun
机构信息
Key Laboratory of Industrial Microbiology, Ministry of Education and Tianjin City, College of Biotechnology, Tianjin University of Science and Technology, Tianjin 300457, PR China.
Key Laboratory of Industrial Microbiology, Ministry of Education and Tianjin City, College of Biotechnology, Tianjin University of Science and Technology, Tianjin 300457, PR China.; College of Life Sciences, Wuhan University of Science and Technology, Wuhan 430081, PR China..
出版信息
Cell Signal. 2017 Feb;31:87-95. doi: 10.1016/j.cellsig.2017.01.003. Epub 2017 Jan 7.
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.
HOTAIR是一种在癌组织中高表达的长链非编码RNA，是一种负性预后因子，然而HOTAIR在癌症中表达上调的机制仍不清楚。在本研究中，我们在乳腺癌细胞MCF7和T47D中研究了HOTAIR转录的调控。我们发现，当RhoC-ROCK信号被特异性siRNA或化学抑制剂干扰时，HOTAIR的表达会下调。此外，发现MRTF-A和SRF会影响HOTAIR的表达。HOTAIR启动子活性被证明以依赖CArG盒的方式受RhoC-MRTF-A-SRF信号调控。此外，鉴定出MRTF-A与HOTAIR启动子存在物理相互作用，并且MRTF-A过表达增强了RNA聚合酶II与HOTAIR启动子的结合。综上所述，我们的结果表明HOTAIR在乳腺癌细胞中受RhoC-MRTF-A-SRF信号通路调控。
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