MicroRNA-98 and microRNA-214 post-transcriptionally regulate enhancer of zeste homolog 2 and inhibit migration and invasion in human esophageal squamous cell carcinoma

Molecular Cancer

Research

Bai-Ling Li¹  Chong-Wen Zhuang²  Zhi-Yong Zeng²  De-Jun Gong³  Shu-Gang Wang⁴  Sheng-Dong Huang⁵  Yang Yuan⁵  He-Zhong Cheng⁶ 

[1] Department of Cardiothoracic Surgery, Changhai Hospital, Shanghai, P.R. China;Department of Cardiothoracic Surgery, Fuzhou General Hospital of Nanjing Command, PLA., Fujian, P.R. China;Department of Pathology, Changhai Hospital, Second Military Medical University, Shanghai, P.R. China;Department of Pathology, Fuzhou General Hospital of Nanjing Command, PLA, Fujian, P.R. China;Institute of Cardiothoracic Surgery, Changhai Hospital, 168, Changhai Rd., Shanghai, P. R. China;Institute of Cardiothoracic Surgery, Changhai Hospital, 168, Changhai Rd., Shanghai, P. R. China;Department of Cardiothoracic Surgery, Changhai Hospital, Shanghai, P.R. China;

关键词: MiR-98;    MiR-214;    EZH2;    ESCC;    Migration;    Invasion;   

DOI  :  10.1186/1476-4598-11-51

 received in 2012-05-05, accepted in 2012-07-26,  发布年份 2012

来源: Springer

【 摘 要 】

BackgroundThe enhancer of zeste homolog 2 (EZH2) was found to be overexpressed and associated with tumor metastasis in esophageal squamous cell carcinoma (ESCC). On the other hand, it was reported that miR-26a, miR-98, miR-101, miR-124, miR-138 and miR-214 could inhibit the expression of EZH2 in some tumors. However, the role of miRNAs in the regulation of EZH2 expression in human ESCC has not been documented. The aim of this study was to determine the role of these miRNAs in the regulation of tumor metastasis via EZH2 overexpression in human ESCC.Methods and resultsThe expression of these miRNAs and EZH2 mRNA were examined by qPCR and the expression of EZH2 protein was detected by western blot. The role of these miRNAs in migration and invasion was studied in ESCC cell line (Eca109) transfected with miRNA mimics or cotransfected with miRNA mimics and pcDNA-EZH2 plasmid (without the 3’-UTR of EZH2). Through clinical investigation, we found that miR-98 and miR-214 expression was significantly lower in ESCC tissues than in matched normal tissues, and the expression level of miR-98 and miR-214 was inversely correlated to EZH2 protein expression and the clinical features such as pathological grade, tumor stage and lymph node metastasis in ESCC. In Eca109 cells, overexpression of miR-98 and miR-214 significantly inhibited the migration and invasion of ESCC cells, which was reversed by transfection of EZH2.ConclusionsThese findings suggest that decreased expression of miR-98 and miR-214 might promote metastasis of human ESCC by inducing accumulation of EZH2 protein.

【 授权许可】

Unknown   
© Yuan et al.; licensee BioMed Central Ltd. 2012. This article is published under license to BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.