WIP1通过诱导MMP-9和VEGF-C来刺激涎腺腺样囊性癌的迁移和侵袭。
WIP1 stimulates migration and invasion of salivary adenoid cystic carcinoma by inducing MMP-9 and VEGF-C.
作者信息
Tang Ya-ling, Liu Xin, Gao Shi-yu, Feng Hao, Jiang Ya-ping, Wang Sha-sha, Yang Jing, Jiang Jian, Ma Xiang-rui, Tang Ya-jie, Chen Yu, Liang Xin-hua
机构信息
Department of Oral Pathology, West China Hospital of Stomatology (Sichuan University), Chengdu Sichuan 610041, People's Republic of China.
State Key Laboratory of Oral Diseases West China Hospital of Stomatology (Sichuan University), Chengdu Sichuan 610041, People's Republic of China.
出版信息
Oncotarget. 2015 Apr 20;6(11):9031-44. doi: 10.18632/oncotarget.3320.
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.
野生型p53诱导磷酸酶1（WIP1）是一种在多种人类癌症中过表达的癌基因。在此，我们证明WIP1沉默可降低基质金属蛋白酶-9（MMP-9）和血管内皮生长因子C（VEGF-C）的表达以及涎腺腺样囊性癌（ACC）细胞的迁移和侵袭能力。MMP-9或VEGF-C的过表达可恢复WIP1敲低细胞的迁移和侵袭能力，表明MMP-9和VEGF-C是WIP1信号通路的下游靶点。Wnt/β-连环蛋白通路的靶点细胞周期蛋白D1和c-Myc的水平因WIP1沉默而显著降低。此外，WIP1表达与ACC患者的转移和预后以及ACC组织中的MMP-9或VEGF-C呈正相关。
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