VHL promotes immune response against renal cell carcinoma via NF-κB–dependent regulation of VCAM-1
Author
Labrousse Arias, David; Martínez Alonso, Emma; Corral-Escariz, María; Bienes Martínez, Raquel; Berridy, Jaime; Serrano-Oviedo, Leticia; Conde, Elisa; García Bermejo, María Laura; Giménez Bachs, José M.; Salinas-Sánchez, Antonio S.; Sánchez Prieto, Ricardo; Yao, Masahiro; Lasa Benito, Marina Paloma; Calzada, María J.Entity
UAM. Departamento de BioquímicaPublisher
Rockefeller University PressDate
2017-02-24Citation
10.1083/jcb.201608024
Journal of Cell Biology 216.3 (2017): 835-847
ISSN
1540-8140 (online); 0021-9525 (print)DOI
10.1083/jcb.201608024Funded by
This work was supported by grants from the Instituto de Salud Carlos III (co-funded by the European Union and Fondo Europeo de Desarrollo Regional; grants PI16/02166 and PIE13/00041), a grant from Red Cardiovascular (RD12/0042/0065 to M.J. Calzada), and a grant from Ministerio de Economía y competitividad (SAF2015- 64215R to R. Sánchez-Prieto)Project
Gobierno de España. PI16/02166; Gobierno de España. PI13/00041Editor's Version
https://doi.org/10.1083/jcb.201608024Subjects
MedicinaRights
© 2017 Labrousse-Arias et alEsta obra está bajo una licencia de Creative Commons Reconocimiento-NoComercial-CompartirIgual 4.0 Internacional.
Abstract
Vascular cell adhesion molecule 1 (VCAM-1) is an adhesion molecule assigned to the activated endothelium mediating immune cells adhesion and extravasation. However, its expression in renal carcinomas inversely correlates with tumor malignancy. Our experiments in clear cell renal cell carcinoma (ccRCC) cell lines demonstrated that von Hippel Lindau (VHL) loss, hypoxia, or PHD (for prolyl hydroxylase domain-containing proteins) inactivation decreased VCAM-1 levels through a transcriptional mechanism that was independent of the hypoxia-inducible factor and dependent on the nuclear factor κB signaling pathway. Conversely, VHL expression leads to high VCAM-1 levels in ccRCC, which in turn leads to better outcomes, possibly by favoring antitumor immunity through VCAM-1 interaction with the α4β1 integrin expressed in immune cells. Remarkably, in ccRCC human samples with VHL nonmissense mutations, we observed a negative correlation between VCAM-1 levels and ccRCC stage, microvascular invasion, and symptom presentation, pointing out the clinical value of VCAM-1 levels as a marker of ccRCC progression
Files in this item
Google Scholar:Labrousse Arias, David
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Martínez Alonso, Emma
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Corral-Escariz, María
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Bienes Martínez, Raquel
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Berridy, Jaime
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Serrano-Oviedo, Leticia
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Conde, Elisa
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García Bermejo, María Laura
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Giménez Bachs, José M.
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Salinas-Sánchez, Antonio S.
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Sánchez Prieto, Ricardo
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Yao, Masahiro
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Lasa Benito, Marina Paloma
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Calzada, María J.
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