Journal
NATURE CELL BIOLOGY
Volume 21, Issue 5, Pages 627-+Publisher
NATURE PUBLISHING GROUP
DOI: 10.1038/s41556-019-0309-2
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Funding
- 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]
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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.
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