Micro RNA ‐128 promotes apoptosis in lung cancer by directly targeting NIMA ‐related kinase 2

Background Micro RNA ‐128 (mi R ‐128) serves as a regulator by inducing cancer cell apoptosis, differentiation, the epithelial‐to‐mesenchymal transition process, and tumor growth by mediating different targets. NIMA ‐related kinase 2 ( NEK 2) is aberrantly expressed in lung cancer. The miR‐128/ NEK 2 pathway has been reported to predict prognosis in colorectal cancer; however, the determination of a relationship between miR‐128 and NEK2 in lung cancer has remained elusive. We explored the association between mi R ‐128 and NEK 2 in lung cancer. Methods Mi R ‐128 and NEK 2 expression were examined in 15 lung cancer tissues by real time‐ PCR . Lung cancer SK‐MES ‐1 cells were transfected with mi R ‐128 mimic, an inhibitor or a negative control. Mi R ‐128 and NEK 2 expression levels were detected using quantitative real time ‐PCR and Western blot. SK‐MES ‐1 cell apoptosis was performed by flow cytometry. Results Compared to adjacent non‐tumor tissues, mi R ‐128 was downregulated and NEK 2 was upregulated in 15 lung cancer tissues. Lung cancer SK‐MES ‐1 cells transfected with mi R ‐128 mimic induced a higher apoptotic rate than those transfected with the negative control. Dual luciferase assay further confirmed that NEK 2 was a direct target of mi R ‐128 in lung cancer, and transfection with mi R ‐128 mimic could decrease the NEK 2 protein level while the mi R ‐128 inhibitor increased NEK 2 expression. Finally, the apoptotic effect of lung cancer cells induced by mi R ‐128 mimic could be reversed by NEK 2 overexpression. Conclusions NEK 2 was regulated by mi R ‐128 in lung cancer and mi R ‐128 induced lung cancer cell apoptosis by mediating NEK 2 expression.