| Background: Epithelial-to-mesenchymal transition (EMT), a process bywhich tumor cell loses the epithelial polarity and acquires a fibroblastoidphenotype, is a vital event during tumor progression. Emerging evidencehave suggested that aberrant expression of cadherins and (or) cadherinswitching, are one of the most important events in the EMT of cancer cells.VE-Cadherin has been observed in certain types of carcinoma. Especially,it was found induced during TGF-β–mediated EMT in breast cancer cells.Here, we analyzed VE-Cadherin expression and function in the EMT oflung cancer cell lines.Methods: VE-Cadherin and N-Cadherin expression in three lung cancercell lines (PG, NCI-H460, A549) were examined with western blot.NCI-H460cells were selected as a target for VE-Cadherin knock-downwith siRNA. Then, the effects of VE-Cadherin on cell migration andinvasion of NCI-H460cells were analyzed with transwell assay, and theeffects on E-Cadherin and N-Cadherin expression were analyzed usingimmunostaining or western blot. In addition, a hypoxic condition assay wasperformed to investigate its impact on VE-Cadherin expression in NCI-H460cells.Results: VE-Cadherin was aberrantly expressed in all three lung cancer celllines (expression trend: PG> NCI-H460> A549), consistent withN-Cadherin expressed in a similar trend. The association betweenVE-cadherin and P120catenin in NCI-H460cell was identified as the sameinteraction as the normal. Inhibition of VE-cadherin expression by siRNAwas tested to reduce migration and invasion of NCI-H460cells in vitro,accompanied by a decrease in N-cadherin and an increase in E-cadherin.Hypoxia induced upregulation of VE-cadherin expression and aspindle-like morphology suggest that NCI-H460cells may underwent anEMT.Conclusions: Our data provides evidence that VE-Cadherin maybeinvolved in the EMT contributing to enhanced metastasis potential ofNSCLC cell. It suggests that VE-cadherin is a potential molecular target inthe treatment of NSCLC. |
PDF Full Text Request