Epithelial-mesenchymal plasticity in carcinoma metastasis

被引:956
作者
Tsai, Jeff H. [1 ]
Yang, Jing [1 ,2 ]
机构
[1] Univ Calif San Diego, Sch Med, Dept Pharmacol, La Jolla, CA 92093 USA
[2] Univ Calif San Diego, Sch Med, Dept Pediat, La Jolla, CA 92093 USA
基金
美国国家卫生研究院;
关键词
epithelial-mesenchymal transition (EMT); mesenchymal-epithelial transition (MET); carcinoma metastasis; extravasation; intravasation; invasion; tumor dormancy; CIRCULATING TUMOR-CELLS; E-CADHERIN GENE; TRANSCRIPTION FACTOR SNAIL; NEGATIVE FEEDBACK LOOP; BREAST-CANCER CELLS; NF-KAPPA-B; MIR-200; FAMILY; COLORECTAL-CANCER; STEM-CELLS; INVADOPODIA FORMATION;
D O I
10.1101/gad.225334.113
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
Tumor metastasis is a multistep process by which tumor cells disseminate from their primary site and form secondary tumors at a distant site. Metastasis occurs through a series of steps: local invasion, intravasation, transport, extravasation, and colonization. A developmental program termed epithelial-mesenchymal transition (EMT) has been shown to play a critical role in promoting metastasis in epithelium-derived carcinoma. Recent experimental and clinical studies have improved our knowledge of this dynamic program and implicated EMT and its reverse program, mesenchymal-epithelial transition (MET), in the metastatic process. Here, we review the functional requirement of EMT and/or MET during the individual steps of tumor metastasis and discuss the potential of targeting this program when treating metastatic diseases.
引用
收藏
页码:2192 / 2206
页数:15
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