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miR-29a suppresses IL-13-induced cell invasion by inhibiting YY1 in the AKT pathway in lung adenocarcinoma A549 cells
miR-29a suppresses IL-13-induced cell invasion by inhibiting YY1 in the AKT pathway in lung adenocarcinoma A549 cells
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miR-29a suppresses IL-13-induced cell invasion by inhibiting YY1 in the AKT pathway in lung adenocarcinoma A549 cells
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miR-29a suppresses IL-13-induced cell invasion by inhibiting YY1 in the AKT pathway in lung adenocarcinoma A549 cells
miR-29a suppresses IL-13-induced cell invasion by inhibiting YY1 in the AKT pathway in lung adenocarcinoma A549 cells

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miR-29a suppresses IL-13-induced cell invasion by inhibiting YY1 in the AKT pathway in lung adenocarcinoma A549 cells
miR-29a suppresses IL-13-induced cell invasion by inhibiting YY1 in the AKT pathway in lung adenocarcinoma A549 cells
Journal Article

miR-29a suppresses IL-13-induced cell invasion by inhibiting YY1 in the AKT pathway in lung adenocarcinoma A549 cells

2018
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Overview
IL-13 is a proinflammatory cytokine associated with multiple pathological conditions and the promotion of metastasis in lung cancer. Previous studies have demonstrated that IL-13 and YY1 are associated with PI3K/AKT signaling. In addition, miR-29a has been found to play a critical role in cell invasion in lung cancer. However, the molecular mechanism of miR-29a underlying its involvement in IL-13-induced lung cancer cell invasion remains largely unknown. In the present study, we aimed to investigate the role of miR-29a in cell invasion mediated by IL-13 in lung cancer. By using MTT and wound-scratch assays, we assessed cell proliferation and migration induced by IL-13, and identified activation of the PI3K/AKT/YY1 pathway. Inhibition of PI3K/AKT by LY294002 downregulated IL-13-induced YY1 expression. Furthermore, we found that miR-29a directly targets YY1 and suppressed its expression in lung cancer. By using MTT, flow cytometry and Transwell assays, overexpression of miR-29a restricted both YY1 and N-cadherin expression, and inhibited IL-13-induced invasion of lung cancer A549 cells. Taken together, these findings demonstrate that PI3K/AKT/YY1 is involved in the regulation of lung cancer cell behavior induced by IL-13, and miR-29a represents a promising therapeutic target.