Abstract
Abstract Transforming growth factor-β (TGF-β)-induced epithelial-mesenchymal transition (EMT) has been reported to be related to pathogenesis of various diseases including lung cancer and idiopathic pulmonary fibrosis (IPF). Recently, microRNAs (miRNA) have been recognized as a new class of genes involved in human tumorigenesis. MiR-23a/24/27a is a miRNA cluster located in 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 of these miRNAs and TGF-β/Smad signaling was evaluated. We found that miR-23a could be regulated by TGF-β1 in a Smad-dependent manner in A549 lung adenocarcinoma cells originated by type II pneumocyte showing the EMT phenomenon. Knockdown of miR-23a partially restored E-cadherin expression under the condition of TGF-β1 stimulation. In contrast, overexpression of miR-23a could suppress E-cadherin expression and stimulate EMT. Furthermore, A549 cells with overexpressed miR-23a were more resistant to gefitinib than the parental cells. These findings suggested that miR-23a regulates TGF-β-induced EMT by targeting E-cadherin in pulmonary epithelium cells and may be useful as a new therapeutic target in pulmonary diseases including NSCLC and IPF. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 103rd Annual Meeting of the American Association for Cancer Research; 2012 Mar 31-Apr 4; Chicago, IL. Philadelphia (PA): AACR; Cancer Res 2012;72(8 Suppl):Abstract nr 2298. doi:1538-7445.AM2012-2298
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