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Shp2 is required in EMT induced by IL-6 in breast cancer cells
Sun Xuan #,Zhang Jie,Wang Zhiyong,Ji Wei,Tian Ran,Zhang Fei,Niu Ruifang *
Key Laboratory of Cancer Prevention and Therapy, Tianjin Medical University Cancer Institute and Hospital, Tianjin 300060, China
*Correspondence author
#Submitted by
Subject:
Funding: Changjiang Scholars and Innovative Research Team （No.IRT_14R40), Specialized Research Fund for the Doctoral Program of Higher Education）
Opened online:23 December 2016
Accepted by: none
Citation: Sun Xuan,Zhang Jie,Wang Zhiyong.Shp2 is required in EMT induced by IL-6 in breast cancer cells[OL]. [23 December 2016] http://en.paper.edu.cn/en_releasepaper/content/4714649
 
 
Accumulative evidence demonstrates that protein tyrosine phosphatase Shp2 functions as a powerful tumor promoter in many types of cancers. Abnormal expression of Shp2 has been implicated in many human malignancies. Overexpression of Shp2 in cancer tissues is correlated with cancer metastasis, resistance to targeted therapy, and poor prognosis. The well-known function of Shp2 is its positive role in regulating cellular signaling initiated by growth factors and cytokines, including interleukin-6 (IL-6). Several recent studies have shown that Shp2 is required for epithelial-mesenchymal transition (EMT) triggered by growth factors. However, whether Shp2 is involved in IL-6-signaling-promoted breast cancer EMT and progression remains undefined. In this study, we showed that exogenous and endogenous IL-6 can enhance breast cancer invasion and migration through the promotion of EMT. IL-6 also induces activation of Erk1/2 and phosphorylation of Shp2. Knockdown of Shp2 inhibited IL-6-induced downregulation of E-cadherin, and IL-6 promoted cell migration and invasion. Moreover, by using Shp2 phosphatase mutants, phosphor-tyrosine mimicking, and deficiency mutants, we provided evidence that the phosphatase activity of Shp2 and its tyrosine phosphorylation are necessary for IL-6-induced downregulation of E-cadherin and phosphorylation of Erk1/2. Our findings uncover an important function that links Shp2 to IL-6-promoted breast cancer progression.
Keywords:Shp2; EMT; IL-6; Invasion; breast cancer
 
 
 

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