Abstract:
Objective To investigate the expression of miR-1290 in non-small cell lung cancer (NSCLC) tissues and its regulation mechanism.
Methods This study evaluated 41 NSCLC patients enrolled in The First Hospital of Shuangliu from June 2014 to 2017. The expression of miR-1290 in NSCLC tissues, adjacent normal tissues, two NSCLC cell lines (A549 and H460), and one normal bronchial epithelial cell line (BEAS-2B) was evaluated by real-time quantitative PCR (qPCR). qPCR and Western blot were conducted to detect the expression of IRF2 mRNA and protein in cancer tissues and adjacent normal tissues. A549 and H460 cells were divided into three groups: miR- 1290 mimic (transfected with miR-1290 mimic), miR-1290 inhibit (transfected with miR-1290 inhibitor), and miR-1290 NC (blank control). At 24, 48, 72, and 96 h after transfection, cell proliferation, colony formation, and invasion ability were detected by CCK-8, colony forming, and Transwell assays, respectively. Luciferase activity was detected and analyzed with a dual-luciferase reporter system. IRF2 mRNA expression in A549 and H460 cells with different miR-1290 expression was detected by qPCR.
Results MiR-1290 expression levels were remarkably upregulated in NSCLC tissues compared with adjacent normal tissues. In addition, compared to adjacent normal tissues, the mRNA and protein expression of IRF2 was significantly downregulated in NSCLC tissues (all P < 0.05). There was an obvious negative correlation between miR-1290 and IRF mRNA and protein expression in NSCLC tissues (P < 0.05). Moreover, higher miR-1290 expression levels were positively associated with lymph node metastasis and an advanced tumor stage (Ⅲ/Ⅳ stage) (all P < 0.05). Functional assays showed that upregulated miR-1290 expression in NSCLC cells enhanced cell proliferation, cell colony formation, and invasion capacities in vitro, while downregulated miR-1290 expression had the opposite effects. Luciferase reporter gene assays revealed that IRF2 is a direct target gene of miR-1290. In both A549 and H460 cells, upregulated miR-1290 expression could depress the expression of IRF2 mRNA and protein; these effects were reversed by downregulating miR-1290.
Conclusions MiR-1290 is upregulated in NSCLC tissues and cells and enhances tumor proliferation and invasion by targeting IRF2 in NSCLC.