Abstract: Objective To explore the effect of silencing NEK2 on the biological behavior of non-small cell lung cancer (NSCLC) cells and its possible mechanism. Methods A total of 27 pairs of NSCLC and adjacent normal tissues were collected, the expression level of NEK2 in those tissues were detected immunohistochemically, and the clinicopathological data were collected. Bioinformatics methods were performed to analyze the expression level and the prognostic value of NEK2 in lung adenocarcinoma. NCI-H1299 and A549 cells were transfected with siRNA to knock down the expression of NEK2 in vitro, and the knockdown efficiency was assessed by Western blotting and qPCR experiments. CCK-8 was used to measure the proliferation rate of cells, and flow cytometry was used to detect the cell apoptosis and cell cycle. Western blotting was used to detect the expression levels of Wnt signaling pathway related proteins. Results The expression level of NEK2 in lung adenocarcinoma tissues was significantly higher than that in the adjacent tissues, and its expression level in the ⅡB-ⅢB group was significantly higher than that in the IA-ⅡA group. The data obtained from the TCGA database also showed that the expression level of NEK2 in patients with lung adenocarcinoma was significantly higher than that in patients of the corresponding control group, and that its high expression level was significantly associated with a poor prognosis. Transfection of NEK2 siRNA significantly inhibited the proliferation and enhanced the apoptosis of NCI-H1299 and A549 cells, made the cells been arrested in the G0 / G1 phase. In addition, the expression levels of Wnt and β-catenin were significantly lower in the NCI-H1299 and A549 cells transfected with NEK2 siRNA, while the expression level of p-GSK3β was higher. Conclusion Silencing of NEK2 by siRNA can inhibit the proliferation of non-small cell lung cancer cells, the mechanism may relate to the promotion of cell apoptosis and cell cycle arrest through the inhibition of the Wnt / β-catenin pathway.

Key words: non-small cell lung cancer, NEK2, cell proliferation, Wnt / β-catenin