作者: Han Xu , Mengquan Li , Yue Zhou , Feng Wang , Xiangke Li
DOI: 10.1007/S13277-015-3709-3
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摘要: Numerous studies have shown that S100A4 acquires its metastasis-promoting effects via inducing epithelial-mesenchymal transition (EMT). However, role and mechanism in EMT breast cancer had not been clearly elucidated. Herein, we showed the knockdown of expression cell lines, MDA-MB-231 MDA-MB-468, inhibited only invasion ability greatly, but also occurrence significantly. In addition, could decrease MMP2, a promoter mediator processes cancer. Above all, restoring MMP2 MDA-MB-468 rescue by S100A4, reverse suppressed S100A4. summary, our results indicated promote cells EMT, more importantly, it participate regulating Therefore, be candidate biomarker for defining metastasis useful target therapy.