Apelin-driven endothelial cell migration sustains intestinal progenitor cells and tumor growth.

Détails

ID Serval
serval:BIB_998EFE1BCFC2
Type
Article: article d'un périodique ou d'un magazine.
Collection
Publications
Institution
Titre
Apelin-driven endothelial cell migration sustains intestinal progenitor cells and tumor growth.
Périodique
Nature cardiovascular research
Auteur⸱e⸱s
Bernier-Latmani J., Cisarovsky C., Mahfoud S., Ragusa S., Dupanloup I., Barras D., Renevey F., Nassiri S., Anderle P., Squadrito M.L., Siegert S., Davanture S., González-Loyola A., Fournier N., Luther S.A., Benedito R., Valet P., Zhou B., De Palma M., Delorenzi M., Sempoux C., Petrova T.V.
ISSN
2731-0590 (Electronic)
ISSN-L
2731-0590
Statut éditorial
Publié
Date de publication
05/2022
Peer-reviewed
Oui
Volume
1
Numéro
5
Pages
476-490
Langue
anglais
Notes
Publication types: Journal Article
Publication Status: 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.
Pubmed
Création de la notice
24/05/2022 13:15
Dernière modification de la notice
08/06/2022 6:36
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