Long non-coding RNA LINC00525 promotes the non-small cell lung cancer progression by targeting miR-338-3p/IRS2 axis.

Long non-coding RNA LINC00525 has been reported to be upregulated in non-small cell lung cancer (NSCLC), however, its biological roles and underlying mechanism involved in modulation of NSCLC remain largely unclear. Real-time PCR were performed to determine the expression of LINC00525 and miR-338-3p in NSCLC tissues and cell lines. Cell proliferation was detected by Cell Counting Kit-8 (CCK-8) and colony-formation assays. Cell migration and invasion were determined by wound healing and transwell invasion assays, respectively. Luciferase reporter and RNA immunoprecipitation (RIP) assays were applied to detect the interactions between molecules. The protein expression was measured by Western blot. Xenograft tumor was established to determine the effect of LINC00525 on NSCLC growth in vivo. LINC00525 expression was significantly upregualted in NSCLC tissues and cell lines, and correlated with poor prognosis. LINC00525 depletion inhibited the proliferation, migration and invasion in NSCLC cell line A549 and SPC-A1 cells. In vivo study further confirmed that LINC00525 knockdown inhibited tumor growth in nude model. Mechanically, LINC00525 served as a molecular sponge for miR-338-3p, and modulated expression of endogenous miR-338-3p-targeted insulin receptor substrate 2(IRS2). These findings indicated that LINC00525 might be the potential target for NSCLC treatment.