期刊
CELL CYCLE
卷 10, 期 17, 页码 2865-2873出版社
TAYLOR & FRANCIS INC
DOI: 10.4161/cc.10.17.17188
关键词
EMT; metastable EMT; TS cells; claudin-low breast cancer; EMT and stemness; epigenetics; MAP3K4; CBP; histone acetylation
类别
资金
- NIH [GM30324, DK37871, GM007040]
- University Cancer Research Fund
Epithelial-mesenchymal transition (EMT) is an essential developmental program that becomes reactivated in adult tissues to promote the progression of cancer. EMT has been largely studied by examining the beginning epithelial state or the ending mesenchymal state without studying the intermediate stages. Recent studies using trophoblast stem (TS) cells paused in EMT have defined the molecular and epigenetic mechanisms responsible for modulating the intermediate metastable stages of EMT. Targeted inactivation of MAP3K4, knockdown of CBP or overexpression of SNAI1 in TS cells induced similar metastable phenotypes. These TS cells exhibited epigenetic changes in the histone acetylation landscape that cause loss of epithelial maintenance while preserving self-renewal and multipotency. A similar phenotype was found in claudin-low breast cancer cells with properties of EMT and stemness. This intersection between EMT and stemness in TS cells and claudin-low metastatic breast cancer demonstrates the usefulness of developmental EMT systems to understand EMT in cancer.
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