Objective  To explore the impact of vascular endothelial cadherin(VE-cadherin) on the invasion and metastasis of non-small cell lung cancer(NSCLC) cells and related mechanism.

Methods  Immunohistochemical staining and RT-PCR were used to detect the expression of VE-cadherin in NSCLC and adjacent tissues. The expression of VE-cadherin in NSCLC cell lines was detected by Western blot. We evaluated the invasion and migration abilities of NCI-H460 cells after VE-cadherin silencing by Transwell assay. Immunofluorescent staining and immunoprecipitation were performed to detect the location and connection of VE-cadherin and P120catenin(P120ctn), respectively.

Results  VE-cadherin expression was higher in NSCLC tissues than that in the matched adjacent tissues, and was associated with smoking history and lymph node metastasis(P<0.05). VE-cadherin was expressed in PG, NCI-H460 and A549 lung cancer cell lines at different expression levels. Silencing VE-cadherin in NCI-H460 cells reduced the cell abilities of invasion and migration, and hypoxia upregulated VE-cadherin expression. VE-cadherin co-localized with P120ctn at cell-cell contacts.

Conclusion  VE-cadherin is correlated with the enhanced invasive and metastatic potential of NSCLC, which may be attributed to hypoxia signal activation and P120ctn mediation.