WIP1 stimulates migration and invasion of salivary adenoid cystic carcinoma by inducing MMP-9 and VEGF-C.
WIP1 stimulates migration and invasion of salivary adenoid cystic carcinoma by inducing MMP-9 and VEGF-C.
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WIP1通过诱导MMP-9和VEGF-C刺激唾液腺腺样囊性癌的迁移和侵袭
DOI：
10.18632/oncotarget.3320
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发表时间：
2015-04-20
期刊：
影响因子：
--
通讯作者：
Liang XH
中科院分区：
文献类型：
--
作者：
Tang YL;Liu X;Gao SY;Feng H;Jiang YP;Wang SS;Yang J;Jiang J;Ma XR;Tang YJ;Chen Y;Liang XH
野生型P53诱导的磷酸酶1(Wip1)是一种在多种人类肿瘤中高表达的癌基因。在这里，我们证明Wip1沉默减少了基质金属蛋白酶-9和血管内皮生长因子-C的表达，以及涎腺腺样囊性癌(ACC)细胞的迁移和侵袭。过表达的基质金属蛋白酶9和血管内皮生长因子C恢复了Wip1基因敲除细胞的迁移和侵袭，表明基质金属蛋白酶9和血管内皮生长因子C是Wip1信号转导的下游靶点。Wip1沉默可显著降低Wnt/β-catenin通路靶点细胞周期蛋白D1和c-Myc的表达水平。此外，Wip1的表达与ACC患者的转移和预后呈正相关，与ACC组织中的基质金属蛋白酶-9和血管内皮生长因子-C呈正相关。
The wild-type p53 induced phosphatase 1 (WIP1) is an oncogene overexpressed in a variety of human cancers. Here, we demonstrated that WIP1 silencing reduced MMP-9 and VEGF-C expression as well as migration and invasion of salivary adenoid cystic carcinoma (ACC) cells. Overexpression of MMP-9 or VEGF-C restored migration and invasion in WIP1 knockdown cells, indicating that MMP-9 and VEGF-C are downstream targets of WIP1 signaling. Levels of cyclin D1 and c-Myc, targets of Wnt/β-catenin pathway, were significantly decreased by WIP1 silencing. In addition, WIP1 expression was positively associated with metastasis and prognosis of ACC patients as well as with MMP-9 or VEGF-C in ACC tissues.
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影响因子：
3.8
作者：
Rauta, J;Alarmo, EL;Kallioniemi, A
通讯作者：
Kallioniemi, A
影响因子：
14.9
作者：
Douarre C;Mergui X;Sidibe A;Gomez D;Alberti P;Mailliet P;Trentesaux C;Riou JF
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Riou JF
影响因子：
--
作者：
Mehner C;Hockla A;Miller E;Ran S;Radisky DC;Radisky ES
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Radisky ES
影响因子：
2.9
作者：
Hayashi R;Tanoue K;Durell SR;Chatterjee DK;Jenkins LM;Appella DH;Appella E
通讯作者：
Appella E
影响因子：
14.9
作者：
Kucher, Ulrike;Schwarze, Uwe Y.;Dobsak, Toni;Heimel, Patrick;Bosshardt, Dieter D.;Kneissel, Michaela;Gruber, Reinhard
通讯作者：
Gruber, Reinhard