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01.12.2016 | Primary research | Ausgabe 1/2016 Open Access

Cancer Cell International 1/2016

MicroRNA-23a regulates epithelial-to-mesenchymal transition in endometrial endometrioid adenocarcinoma by targeting SMAD3

Zeitschrift:
Cancer Cell International > Ausgabe 1/2016
Autoren:
Ping Liu, Chao Wang, Chengbin Ma, Qiongwei Wu, Wenying Zhang, Guoying Lao
Wichtige Hinweise

Electronic supplementary material

The online version of this article (doi:10.​1186/​s12935-016-0342-1) contains supplementary material, which is available to authorized users.
Ping Liu and Chao Wang contributed equally to this work

Abstract

Background

To investigate the role of total cellular microRNA (miRNA) in regulating epithelial-to-mesenchymal transition (EMT) during human endometrial endometrioid adenocarcinoma (EEC).

Methods

A miRCURY LNA microRNA array was used to evaluate the miRNA profiles of human EEC tissues and corresponding nontumorous endometriums. An in vitro model of TGF-β induced EMT in HEC-1-A cells was used to investigate the role of miRNAs in the EEC during EMT. The expression of SMAD3, SMAD5, and a panel of EMT markers was detected by Western blot and quantitative PCR.

Results

The results of miRNA profiling in human EEC tissues and corresponding nontumorous endometriums demonstrated that miR-23a expression was down-regulated. Using bioinformatics, we identified SMAD3 or SMAD5 maybe as a predicted target of miR-23a. The results of luciferase reporter assay showed miR-23a directly targets and down-regulates human SMAD3 protein levels, not SMAD5 protein levels. Furthermore, overexpression of miR-23a in HEC-1-A cells increased E-cadherin expression and decreased the expression of vimentin and alpha smooth muscle actin, markers of mesenchymal cellular phenotype.

Conclusions

Our data provide firm evidence of a role for miR-23a in the direct regulation of EMT through its targeting of SMAD3. Due to its ability to repress the EMT, miR-23a may be a novel target for EER therapeutic intervention.
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