SOX2 promotes tumor metastasis by stimulating epithelial-to-mesenchymal transition via regulation of WNT/β-catenin signal network

被引:188
作者
Li, Xuefei [1 ]
Xu, Yingxi [1 ]
Chen, Yanan [1 ]
Chen, Si [1 ,2 ]
Jia, Xianpei [1 ]
Sun, Tongchao [1 ]
Liu, Yanhua [1 ]
Li, Xiru [3 ]
Xiang, Rong [1 ,4 ]
Li, Na [1 ,4 ]
机构
[1] Nankai Univ, Sch Med, Tianjin 300071, Peoples R China
[2] US FDA, Div Biochem Toxicol, Natl Ctr Toxicol Res, Jefferson, AR 72079 USA
[3] Chinese Peoples Liberat Army Gen Hosp, Dept Gen Surg, Beijing 100853, Peoples R China
[4] Tianjin Key Lab Tumor Microenvironm & Neurovasc R, Tianjin 300071, Peoples R China
关键词
SOX2; Tumor metastasis; EMT; beta-catenin; TGF-beta; 1; BREAST-CANCER CELLS; STEM-CELLS; E-CADHERIN; TIGHT JUNCTIONS; EXPRESSION; PLURIPOTENCY; MECHANISMS; INVASION; PATHWAY; TRAITS;
D O I
10.1016/j.canlet.2013.03.027
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
SOX2 was reported to promote metastasis in various tumor tissues; however the underlying mechanisms remain elusive. Here, we disclosed that SOX2 improves metastasis of breast and prostate cancer cells by promoting epithelial-to-mesenchymal transition (EMT) through WNT/beta-catenin, but not TGF-beta or Snaill signaling. Dual luciferase assay and chromatin immunoprecipitation revealed activation and binding of SOX2 on promoter region of beta-catenin. In addition, SOX2 affects the protein expression levels of DKK3, DVL1 and DVL3, which are regulators or downstream molecules of WNT signaling. Taken together, our findings demonstrated beta-catenin as one of vital downstream molecules that mediate the EMT induced by SOX2. (C) 2013 Elsevier Ireland Ltd. All rights reserved.
引用
收藏
页码:379 / 389
页数:11
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