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DAL-1 attenuates epithelial-to mesenchymal transition in lung cancer.
- Source :
-
Journal of experimental & clinical cancer research : CR [J Exp Clin Cancer Res] 2015 Jan 22; Vol. 34, pp. 3. Date of Electronic Publication: 2015 Jan 22. - Publication Year :
- 2015
-
Abstract
- 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.<br />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.<br />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.<br />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.
- Subjects :
- Adult
Aged
Aged, 80 and over
Biomarkers, Tumor metabolism
Cadherins metabolism
Cell Line, Tumor
Down-Regulation
Endoplasmic Reticulum Chaperone BiP
Humans
Microfilament Proteins genetics
Middle Aged
Neoplasm Metastasis
Vimentin metabolism
beta Catenin metabolism
Adenocarcinoma metabolism
Adenocarcinoma pathology
Epithelial-Mesenchymal Transition
Lung Neoplasms metabolism
Lung Neoplasms pathology
Microfilament Proteins metabolism
Subjects
Details
- Language :
- English
- ISSN :
- 1756-9966
- Volume :
- 34
- Database :
- MEDLINE
- Journal :
- Journal of experimental & clinical cancer research : CR
- Publication Type :
- Academic Journal
- Accession number :
- 25609022
- Full Text :
- https://doi.org/10.1186/s13046-014-0117-2