Background
The epithelial-mesenchymal transition (EMT), featured by abatement of cell-cell contact, is related to exacerbating non-small cell lung cancer (NSCLC) by inducing metastasis. MAL and relevant proteins for vesicle trafficking and membrane link domain 3 (MARVELD3) is a novel tight junction protein participated in the EMT. There is limited information available about the mechanism of MARVELD3 in NSCLC. In this trial, the inhibition effect of MARVELD3 on human NSCLC cells will be discussed.
Conclusions
TGF-β1 induced EMT in human NSCLC cells can be suppressed by MARVELD3 through Wnt/β-catenin signaling pathway. These results indicate that MARVELD3 might be a potential therapeutic modality useful in the treatment of NSCLC.
Methods
MARVELD3 expression was measured in NSCLC tissues and para-carcinoma tissues. The expression of MARVELD3 and EMT-related genes were examined in transforming growth factor (TGF)-β1-induced NSCLC cells. NSCLC cells with MARVELD3-knockdown and overexpressed were established to analyze the relationship between MARVELD3 and EMT and cell migration. The Wnt/β-catenin pathway expression was also analyzed in NSCLC cell models and clinic species.
Results
Lower protein levels of MARVELD3 were observed in NSCLC samples than para-carcinoma specimens, and the decreased expression of MARVELD3 in NSCLC specimens was associated with tumor metastasis. E-Cadherin and MARVELD3 expression was reduced in TGF-β1 treated NSCLC cells, whereas increased Vimentin expression was detected. MARVELD3 changed the EMT-related genes and induced cell migration. In addition, Wnt/β-catenin pathway and target genes, MYC and CCND1, expressions were inhibited in MARVELD3 overexpressed NSCLC cells. Conclusions: TGF-β1 induced EMT in human NSCLC cells can be suppressed by MARVELD3 through Wnt/β-catenin signaling pathway. These results indicate that MARVELD3 might be a potential therapeutic modality useful in the treatment of NSCLC.