期刊
NATURE CELL BIOLOGY
卷 21, 期 5, 页码 627-+出版社
NATURE PUBLISHING GROUP
DOI: 10.1038/s41556-019-0309-2
关键词
-
类别
资金
- NIH [F31CA192461]
- NJCCR
- National Institutes of Health NHLBI [PO1 HL107146]
- Program of Excellence in Glycosciences
- Team Jobie Fund
- Susan G. Komen Foundation [SAC160067]
- Glycomimetics Inc.
- Brewster Foundation
- Department of Defense [BC123187]
- National Institutes of Health [R01CA141062]
- Preclinical Imaging, Genomic Editing and Flow Cytometry Shared Resources of the Rutgers Cancer Institute of New Jersey [P30CA072720]
How disseminated tumour cells engage specific stromal components in distant organs for survival and outgrowth is a critical but poorly understood step of the metastatic cascade. Previous studies have demonstrated the importance of the epithelial-mesenchymal transition in promoting the cancer stem cell properties needed for metastasis initiation, whereas the reverse process of mesenchymal-epithelial transition is required for metastatic outgrowth. Here we report that this paradoxical requirement for the simultaneous induction of both mesenchymal-epithelial transition and cancer stem cell traits in disseminated tumour cells is provided by bone vascular niche E-selectin, whose direct binding to cancer cells promotes bone metastasis by inducing mesenchymal-epithelial transition and activating Wnt signalling. E-selectin binding activity mediated by the alpha 1-3 fucosyltransferases Fut3/Fut6 and Glg1 are instrumental to the formation of bone metastasis. These findings provide unique insights into the functional role of E-selectin as a component of the vascular niche critical for metastatic colonization in bone.
作者
我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。
推荐
暂无数据