MiR-23a regulates TGF-β-induced epithelial-mesenchymal transition by targeting E-cadherin in lung cancer cells | Zendy

Mengru Cao | Zendy; Masahiro Seike | Zendy; Chie Soeno | Zendy; Hideaki Mizutani | Zendy; Kazuhiro Kitamura | Zendy; Yuji Minegishi | Zendy; Rintaro Noro | Zendy; Akinobu Yoshimura | Zendy; Li Cai | Zendy; Akihiko Gemma | Zendy

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MiR-23a regulates TGF-β-induced epithelial-mesenchymal transition by targeting E-cadherin in lung cancer cells

Author(s) -

Mengru Cao,

Masahiro Seike,

Chie Soeno,

Hideaki Mizutani,

Kazuhiro Kitamura,

Yuji Minegishi,

Rintaro Noro,

Akinobu Yoshimura,

Li Cai,

Akihiko Gemma

Publication year - 2012

Publication title -

international journal of oncology

Language(s) - English

Resource type - Journals

SCImago Journal Rank - 1.405

H-Index - 122

ISSN - 1019-6439

DOI - 10.3892/ijo.2012.1535

Subject(s) - epithelial–mesenchymal transition , cancer research , oncogene , microrna , biology , gene knockdown , carcinogenesis , transforming growth factor , smad , gene silencing , lung cancer , a549 cell , cell cycle , cancer , cell , metastasis , microbiology and biotechnology , cell culture , pathology , medicine , gene , genetics

Transforming growth factor-β (TGF-β)-induced epithelial-mesenchymal transition(EMT) has been shown to be related to the pathogenesis of various diseases includinglung cancer. Recently, microRNAs (miRNA) have been recognized as a new class ofgenes involved in human tumorigenesis. MiR-23a/24/27a is a miRNA cluster locatedin chromosome 19p13.12, which can function as an oncogene in several human cancers.In this study, we analyzed miR-23a/24/27a expression in 10 non-small cell cancer(NSCLC) cell lines by real-time PCR analysis. Correlation between expression ofthese miRNAs and TGF-β/Smad signaling was evaluated. We found that miR-23a couldbe regulated by TGF-β1 in a Smad-dependent manner in A549 lung adenocarcinomacells showing the EMT phenomenon. Knockdown of miR-23a partially restored E-cadherinexpression under conditions of TGF-β1 stimulation. In contrast, overexpressionof miR-23a could suppress E-cadherin expression and stimulate EMT. Furthermore,A549 cells with overexpressed miR-23a were more resistant to gefitinib comparedto the parental cells. These findings suggest that miR-23a regulates TGF-β-inducedEMT by targeting E-cadherin in lung cancer cells and may be useful as a new therapeutictarget in NSCLC.

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