Neuroleukin regulates the metastasis of non-small cell lung cancer cells through the Wnt/β-catenin signaling pathway

Purpose: We investigate the mechanisms of neuroleukin (NLK) in the metastasis of non-small cell lung cancer (NSCLC). Methods: A549 cells were separated into an si-NLK group, an NC group, and a control group. The expression of NLK was measured by qRT-PCR. The proliferation of A549 cells was measured using cell cloning and an MTT assay, and the migration ability of the A549 cells was measured using a scratch test, and the invasiveness of A549 cells was tested isomg a Transwell invasion assay. Additionally, immunofluorescence was used to observe the distribution of beta-catenin in the cells, and western blot was applied in measuring the expressions of beta-catenin, cyclin D1, and c-myc. Results: After transfection with NLK-siRNA, the expression of NLK was distinctly decreased compared to the control and NC group (P < 0.05). The proliferation in the si-NLK group was prominently slower than it was in the other two groups (P < 0.05). The cell cloning, migration, and invasiveness abilities in the si-NLK group was markedly decreased compared to the control and NC groups (P < 0.05). A high positive expression of beta-catenin in the nuclei was detected in the control and NC groups. Moreover, in the si-NLK group, it was mainly expressed in the membranes, and the expression showed a downward trend. By comparison with the control and NC groups, the expressions of c-myc, beta-catenin, and cyclin D1 in the si-NLK group were markedly down-regulated (P < 0.05). Conclusions: NLK significantly promotes the metastasis of NSCLC cells by adjusting the Wnt/beta-catenin signaling pathway, which could provide a new target for controlling the metastasis of NSCLC at the gene level.