The Mechanism of Nemo-Like Kinase (NLK) in Non-Small Cell Lung Cancer (NSCLC) Cells by Regulating Vascular Endothelial Growth Factor (VEGF)

Nemo-like kinase (NLK) is abnormally expressed in several tumors, but its role in NSCLC have not been reported. Real time PCR and Western blot were used to assess NLK level in tumor tissues and adjacent tissues of NSCLC. NSCLC cell line A549 cells were divided into three groups; NC
 group and si-NLK group which was transfected with NLK negative control or NLK siRNA respectively followed by analysis of NLK expression by real time PCR and Western blot, cell proliferation by MTT assay, cell migration by cell wound healing assay, cell invasion by transwell chamber and MMP-9
 and VEGF expression by Western blot. The expression of NLK in NSCLC tumor tissue was increased, and the difference was statistically significant compared with adjacent tissues (P <0.05), and it was related to tumor size, degree of differentiation, metastasis and survival time (P
 <0.05). A549 cells showed significantly increased NLK. Transfection of NLK siRNA could significantly inhibit tumor cell proliferation, migration and invasion, and decrease the expression of MMP-9 and VEGF proteins (P <0.05). Elevated NLK level in NSCLC tumor tissues is related
 to clinicopathological characteristics. Decreased the expression of NLK can inhibit VEGF and MMP-9 expression, and inhibit cell function.