Overexpression of miR-1290 contributes to cell proliferation and invasion of non small cell lung cancer by targeting interferon regulatory factor 2.

MicroRNAs are small endogenous non-coding RNAs, which can frequently emerge as regulators in many cancer types. MiR-1290 was found to be abnormally elevated in non small cell lung cancer (NSCLC). However, the underlying molecular mechanism still needs to be investigated. Here, we demonstrated that miR-1290 expression levels were remarkably upregulated in NSCLC tissues compared to adjacent normal tissues. Higher miR-1290 expression levels positively associated with lymph node metastasis and advanced tumor stage. Functional assays showed that upregulated miR-1290 expression in NSCLC cells enhanced cell proliferation, cell colony formation and invasion capacities in vitro. Furthermore, we found that miR-1290 promoted cell proliferation related protein CDK2 and CDK4 expression and enhanced Epithelial-Mesenchymal Transition (EMT) process by downregulating E-cadherin expression and upregulating N-cadherin expression. Bioinformatics analysis and luciferase reporter gene assays revealed that Interferon regulatory factor 2 (IRF2) was a direct target of miR-1290. Overexpression of miR-1290 can degrade IRF2 mRNA and downregulated IRF2 protein expression in NSCLC cells. Upregulated IRF2 could partly rescue the promoting effects induced by miR-1290 overexpression on cell proliferation and invasion of NSCLC. Additionally, we confirmed that reduced miR-1290 expression could suppress tumor growth using a tumor xenograft model in vivo. Thus, we concluded that miR-1290 may serve as a potential target of NSCLC treatment.