miRNA-221 acts as an oncogenic role by directly targeting TIMP2 in non-small-cell lung carcinoma.

MicroRNA-221 (miRNA-221) plays an important role in occurrence and development of tumor. However, expression pattern and role of miRNA-221 in the non-small-cell lung carcinoma (NSCLC) remains poorly understood. In the current study, we explored the roles and the underlying mechanism of miR-221 in NSCLC by gain and loss of function analysis. We found that the expression of miRNA-221 is significantly higher in NSCLC tissues and NSCLC cells compared to normal tissues and cells, respectively (P<0.05). NSCLC cell lines SPCA1 and H1299 were transfected with miRNA-221 mimic or inhibitor, respectively, and then performed to analysis. Experiments indicated that upregulation of miRNA-221 promotes cell proliferation, cell cycle, migration, invasion in SPCA1 cells, while downregulation of miRNA-221 exhibited the opposite role. Tissue inhibitor of metallopeptidases-2 (TIMP2) mRNA or protein levels were downregulated after miRNA-221 overexpression in SPCA1 and H1299 cells, respectively. Furthermore, TIMP2 was identified as a direct target of miRNA-221. In summary, our results indicate that miRNA-221 promotes NSCLC growth and invasion through repressing the expression of TIMP2, which suggest that inhibition of miRNA-221 could be a potential target for the treatment of NSCLC.