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
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
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DOI：
10.3892/ol.2015.3898
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发表时间：
2016-01-01
期刊：
影响因子：
2.9
通讯作者：
Wang, Anxun
中科院分区：
文献类型：
--
作者：
Zhao, Tingting;He, Qianting;Wang, Anxun
我们以前的研究表明，微管相关肿瘤抑制因子1/血管紧张素II 2型受体相互作用蛋白（MTUS 1/ATIP）的下调与舌鳞状细胞癌（TSCC）的分化和预后不良有关，ATIP 1对TSCC具有抗增殖作用。本研究的目的是进一步研究MTUS 1/ATIP 3a在TSCC中的抗癌作用。观察到，与UM 2细胞（具有较低迁移和侵袭能力的TSCC细胞系）相比，UM 1细胞（具有高迁移和侵袭能力的TSCC细胞系）表现出较低的ATIP 3a表达。在UM 1细胞中恢复ATIP 3a表达具有抗增殖作用并抑制迁移和侵袭，而在UM 2细胞中ATIP 3a的敲除促进增殖、迁移和侵袭。ATIP 3a表达的恢复抑制了UM 1细胞中细胞外信号调节激酶1/2（ERK 1/2）的磷酸化以及Snai 2和vimentin的表达，而ATIP 3a的敲低促进了UM 2细胞中ERK 1/2的磷酸化以及Snai 2和vimentin的表达。因此，MTUS 1/ATIP 3a被发现通过ERK 1/2-Snai 2途径抑制TSCC细胞的增殖、迁移和侵袭。
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.