Research Papers:
WIP1 stimulates migration and invasion of salivary adenoid cystic carcinoma by inducing MMP-9 and VEGF-C
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Abstract
Ya-ling Tang1,2, Xin Liu2, Shi-yu Gao2, Hao Feng2, Ya-ping Jiang2, Sha-sha Wang2, Jing Yang2, Jian Jiang2, Xiang-rui Ma2, Ya-jie Tang3, Yu Chen1, Xin-hua Liang2,4
1Department of Oral Pathology, West China Hospital of Stomatology (Sichuan University), Chengdu Sichuan 610041, People’s Republic of China
2State Key Laboratory of Oral Diseases West China Hospital of Stomatology (Sichuan University), Chengdu Sichuan 610041, People’s Republic of China
3Key Laboratory of Fermentation Engineering (Ministry of Education), Hubei University of Technology, Wuhan 430068, People’s Republic of China
4Department of Oral and Maxillofacial Surgery, West China Hospital of Stomatology (Sichuan University), Chengdu Sichuan 610041, People’s Republic of China
Correspondence to:
Xin-hua Liang, e-mail: [email protected], [email protected]
Keywords: wild-type p53 induced phosphatase 1 (WIP1), adenoid cystic carcinoma (ACC), salivary gland, invasion, metastasis
Received: January 09, 2015 Accepted: February 23, 2015 Published: March 06, 2015
ABSTRACT
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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