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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.

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