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Angiotensin II type 2 receptor-interacting protein 3a suppresses proliferation, migration and invasion in tongue squamous cell carcinoma via the extracellular signal-regulated kinase-Snai2 pathway
- Source :
- Oncology Letters. 11:340-344
- Publication Year :
- 2015
- Publisher :
- Spandidos Publications, 2015.
-
Abstract
- Our previous studies demonstrated that the downregulation of microtubule-associated tumor suppressor 1/angiotensin II type 2 receptor-interacting protein (MTUS1/ATIP) is associated with poor differentiation and prognosis in tongue squamous cell carcinoma (TSCC), and that ATIP1 exerts an antiproliferative effect on TSCC. The aim of the present study was to further investigate the anticancer effect of MTUS1/ATIP3a in TSCC. It was observed that UM1 cells (a TSCC cell line with high migration and invasion ability) exhibited lower expression of ATIP3a compared with UM2 cells (a TSCC cell line with lower migration and invasion ability). Restoration of ATIP3a expression in UM1 cells exerted antiproliferative effects and inhibited migration and invasion, whereas knockdown of ATIP3a promoted proliferation, migration and invasion in UM2 cells. Restoration of ATIP3a expression inhibited the phosphorylation of extracellular signal-regulated kinase 1/2 (ERK1/2) and the expression of Snai2 and vimentin in UM1 cells, whereas knockdown of ATIP3a promoted the phosphorylation of ERK1/2 and the expression of Snai2 and vimentin in UM2 cells. Therefore, MTUS1/ATIP3a was found to suppress the proliferation, migration and invasion of TSCC cells via the ERK1/2-Snai2 pathway.
- Subjects :
- 0301 basic medicine
Cancer Research
Pathology
medicine.medical_specialty
biology
Oncogene
Kinase
Cell
Vimentin
Articles
Cell cycle
Angiotensin II
03 medical and health sciences
030104 developmental biology
0302 clinical medicine
medicine.anatomical_structure
Oncology
Downregulation and upregulation
Cell culture
030220 oncology & carcinogenesis
medicine
Cancer research
biology.protein
Subjects
Details
- ISSN :
- 17921082 and 17921074
- Volume :
- 11
- Database :
- OpenAIRE
- Journal :
- Oncology Letters
- Accession number :
- edsair.doi.dedup.....777693807167a04d654085d28fda8559