4.4 Article

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

Journal

ONCOLOGY LETTERS
Volume 11, Issue 1, Pages 340-344

Publisher

SPANDIDOS PUBL LTD
DOI: 10.3892/ol.2015.3898

Keywords

microtubule-associated tumor suppressor 1; angiotensin II type 2 receptor-interacting protein 3a; tongue squamous cell carcinoma; proliferation; migration; invasion

Categories

Funding

  1. National Natural Science Foundation of China [NSFC81072228, NSFC81272953]
  2. Guangdong Natural Science Foundation [S2011020002325]
  3. research fund for the doctoral program of the Ministry of Education [20120171110050]
  4. Fundamental Research Funds for the Central Universities [11ykzd09]
  5. Program for New Century Excellent Talents in University [NCET-10-0857]
  6. Project of Science and Technology of Guangdong Province [2012B031800080]
  7. National Institutes of Health PHS [CA139596]

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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.

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