Apelin-driven endothelial cell migration sustains intestinal progenitor cells and tumor growth.
Journal
Nature cardiovascular research
ISSN: 2731-0590
Titre abrégé: Nat Cardiovasc Res
Pays: England
ID NLM: 9918284280206676
Informations de publication
Date de publication:
May 2022
May 2022
Historique:
entrez:
23
5
2022
pubmed:
24
5
2022
medline:
24
5
2022
Statut:
ppublish
Résumé
Stem and progenitor cells residing in the intestinal crypts drive the majority of colorectal cancers (CRCs), yet vascular contribution to this niche remains largely unexplored. VEGFA is a key driver of physiological and tumor angiogenesis. Accordingly, current anti-angiogenic cancer therapies target the VEGFA pathway. Here we report that in CRC expansion of the stem/progenitor pool in intestinal crypts requires VEGFA-independent growth and remodeling of blood vessels. Epithelial transformation induced expression of the endothelial peptide apelin, directs migration of distant venous endothelial cells towards progenitor niche vessels ensuring optimal perfusion. In the absence of apelin, loss of injury-inducible PROX1+ epithelial progenitors inhibited both incipient and advanced intestinal tumor growth. Our results establish fundamental principles for the reciprocal communication between vasculature and the intestinal progenitor niche and provide a mechanism for resistance to VEGFA-targeting drugs in CRCs.
Identifiants
pubmed: 35602406
doi: 10.1038/s44161-022-00061-5
pmc: PMC7612746
mid: EMS144141
doi:
Types de publication
Journal Article
Langues
eng
Pagination
476-490Subventions
Organisme : Swiss National Science Foundation
ID : 156266
Pays : Switzerland
Organisme : Swiss National Science Foundation
ID : 166161
Pays : Switzerland
Organisme : European Research Council
ID : 725051
Pays : International
Déclaration de conflit d'intérêts
Competing interests TVP receives research funding from Roche for an unrelated project. All other authors declare no conflict of interest.
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