A central role for MeCP2 in the epigenetic repression of miR-200c during epithelial-to-mesenchymal transition of glioma

doi:10.1186/s13046-019-1341-6

HFCAS OpenIR

	A central role for MeCP2 in the epigenetic repression of miR-200c during epithelial-to-mesenchymal transition of glioma
	Bian,Erbao 1,2; Chen,Xueran 3; Xu,Yadi 1,2; Ji,Xinghu 1,2; Cheng,Meng 1,2; Wang,Hongliang 1,2; Fang,Zhiyou 3; Zhao,Bing 1,2
	2019-08-20
发表期刊	Journal of Experimental & Clinical Cancer Research
ISSN	1756-9966
通讯作者	Fang,Zhiyou(z.fang@cmpt.ac.cn) ; Zhao,Bing(aydzhb@126.com)
摘要	AbstractBackgroundThe epithelial-to-mesenchymal transition (EMT) has been linked to the regulation of glioma progression. However, the underlying signaling mechanisms that regulate EMT are poorly understood.MethodsQuantitative real-time PCR (RT-qPCR) and western blot were performed to detect the expression of MeCP2 in glioma tissues and cell lines. MeCP2 functions were tested with cell immunofluorescence staining and western blot. For in vivo experiments, mouse xenograft model was used to investigate the effects of MeCP2 on glioma. ChIP and Co-IP were used to detect the relationships among MeCP2, miR-200c and Suv39H1.ResultsIn this study, we found that MeCP2 was frequently up-regulated in human glioma tissues and cell lines. MeCP2 knockdown remarkably induced cell epithelial phenotype and inhibited mesenchymal marker ZEB1 and ZEB2 in vitro and in vivo. In addition, MeCP2 in glioma tissues was negatively correlated with miR-200c expression, and miR-200c overexpression partially abrogated mesenchymal phenotype induced by MeCP2. More importantly, we showed that MeCP2 recruited H3K9 to the promoter of miR-200c by interacting with SUV39H1, resulting in EMT of glioma cells.ConclusionsThis study for the first time reveals MeCP2 as a novel regulator of EMT in glioma and suggest that MeCP2 inhibition may represent a promising therapeutic option for suppressing EMT in glioma.
关键词	Glioma MeCP2 miR-200c SUV39H1
DOI	10.1186/s13046-019-1341-6
语种	英语
资助项目	[National Natural Science Foundation of China] ; [Natural Science Foundation of Anhui Province] ; [Key Research and Development Plan Project of Anhui Province] ; [College Excellent Youth Talent Support Program in Anhui Province] ; [Academic Funding Project for Top Talents in Colleges and Universities in Anhui Province] ; [Nova Pew Plan of the Second Affiliated Hospital of Anhui Medical University]
WOS记录号	BMC:10.1186/s13046-019-1341-6
出版者	BioMed Central
引用统计
文献类型	期刊论文
条目标识符	http://ir.hfcas.ac.cn:8080/handle/334002/42802
专题	中国科学院合肥物质科学研究院
通讯作者	Fang,Zhiyou; Zhao,Bing
作者单位	1. 2. 3.
推荐引用方式 GB/T 7714	Bian,Erbao,Chen,Xueran,Xu,Yadi,et al. A central role for MeCP2 in the epigenetic repression of miR-200c during epithelial-to-mesenchymal transition of glioma[J]. Journal of Experimental & Clinical Cancer Research,2019,38.
APA	Bian,Erbao.,Chen,Xueran.,Xu,Yadi.,Ji,Xinghu.,Cheng,Meng.,...&Zhao,Bing.(2019).A central role for MeCP2 in the epigenetic repression of miR-200c during epithelial-to-mesenchymal transition of glioma.Journal of Experimental & Clinical Cancer Research,38.
MLA	Bian,Erbao,et al."A central role for MeCP2 in the epigenetic repression of miR-200c during epithelial-to-mesenchymal transition of glioma".Journal of Experimental & Clinical Cancer Research 38(2019).