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

• DOI: 10.3892/or.2018.6352
• Publication Date: 2018-04-04T09:06:38Z
• Authors: Yu Zhang; Shujin He; Renmei Mei; Yurong Kang; Jing Duan; Ran Wei; Chuqi Xiang; Yemeng Wu; Xiangtong Lu; Zhenyu Cai; Lixia Xiong
• Keywords: 0301 basic medicine; Interleukin-13; Lung Neoplasms; Adenocarcinoma of Lung; Articles; Adenocarcinoma; 3. Good health; Gene Expression Regulation, Neoplastic; MicroRNAs; 03 medical and health sciences; A549 Cells; Cell Movement; Humans; Neoplasm Invasiveness; Proto-Oncogene Proteins c-akt; YY1 Transcription Factor; Cell Proliferation; Signal Transduction

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.