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01.12.2012 | Research | Ausgabe 1/2012 Open Access

Molecular Cancer 1/2012

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

Zeitschrift:
Molecular Cancer > Ausgabe 1/2012
Autoren:
Sheng-Dong Huang, Yang Yuan, Chong-Wen Zhuang, Bai-Ling Li, De-Jun Gong, Shu-Gang Wang, Zhi-Yong Zeng, He-Zhong Cheng
Wichtige Hinweise

Electronic supplementary material

The online version of this article (doi:10.​1186/​1476-4598-11-51) contains supplementary material, which is available to authorized users.
Sheng-Dong Huang, Yang Yuan contributed equally to this work.

Competing interests

The authors declare that they have no competing interests.

Authors' contributions

SDH and ZYZ designed research and analyzed data. YY, HZC, BLL, DJG, CWZ and SGW carried out molecular biology studies. YY and HZC wrote the paper. All authors read and approved the final manuscript.

Abstract

Background

The 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 results

The 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.

Conclusions

These findings suggest that decreased expression of miR-98 and miR-214 might promote metastasis of human ESCC by inducing accumulation of EZH2 protein.
Zusatzmaterial
Additional file 1: Figure S1.The expression level of EZH2 protein in ESCC and paired normal tissues. (PDF 12 KB)
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Additional file 2: Figure S2.The expression levels of miRNAs were significantly increased in Eca109 cells transfected with miRNA mimics. (PDF 19 KB)
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Additional file 3: Figure S3.The expression levels of EZH2 was significantly increased in Eca109 cells transfected with pcDNA.EZH2. (PDF 18 KB)
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Authors’ original file for figure 1
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Authors’ original file for figure 2
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Authors’ original file for figure 3
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Authors’ original file for figure 4
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Authors’ original file for figure 5
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Authors’ original file for figure 6
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Literatur
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