DAL-1 attenuates epithelial- to mesenchymal transition in lung cancer

Background: epithelial- to mesenchymal transition (emt) involves in metastasis,causing loss of epithelial polarity. metastasis is the major cause of carcinoma-induced death,but mechanisms are poorly understood. here we identify differentially expressed in adenocarcinoma of the lung-1 (dal-1),a protein belongs to the membrane-associated cytoskeleton protein 4.1 family,as an efficient suppressor of emt in lung cancer. methods: the relationship between dal-1 and emt markers were analyzed by using immunohistochemistry in the clinical lung cancer tissues. quantitative real-time pcr and western blot were used to characterize the expression of the emt indicator mrnas and proteins in dal-1 overexpressed or knockdown cells. dal-1 combined proteins were assessed by co-immunoprecipitation. results: dal-1 levels were strongly reduced even lost in lymph node metastasis and advanced pathological stage of human lung carcinomas. overexpression of dal-1 altered the expression of numerous emt markers,such as e-cadherin,β-catenin vimentin and n-cadherin expression,meanwhile changed the morphological shape of lung cancer cells,and whereas silencing dal-1 had an opposite effect. dal-1 directly combined with e-cadherin promoter and regulated its expression that could be the reason for impairing emt and decreasing cell migration and invasion. strikingly,hspa5 was found as dal-1 direct binding protein. conclusions: these results suggest that tumor suppressor dal-1 could also attenuate emt and be important for tumor metastasis in the early transformation process in lung cancer. © 2015 chen et al.; licensee biomed central.