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Cavin-2 Functions as a Suppressive Regulator in TNF-induced Mesenchymal Stromal Cell Inflammation and Angiogenic Phenotypes
International Journal of Stem Cells
Published online December 31, 2016;  
© 2016 Korean Society for Stem Cell Research.

Bayader Annabi1,2, Alain Zgheib1, Borhane Annabi1

1Laboratoire d’Oncologie Moléculaire, Département de Chimie, Centre de recherche BIOMED, Université du Québec à Montréal, Quebec,
2Département de Physiologie Moléculaire et Intégrative, Faculté de Médecine, Université de Montréal, Montreal, Canada
Correspondence to: Borhane Annabi
Département de Chimie, Université du Québec à Montréal, C.P. 8888, Succ. Centre-ville, Montréal, Québec, Canada, H3C 3P8
Tel: +514-987-3000 ext 7610, Fax: +514-987-0246 E-mail:
; Accepted November 24, 2016.
This is an open-access article distributed under the terms of the Creative Commons Attribution Non-Commercial License ( licenses/by-nc/4.0/), which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.
Tumour necrosis factor (TNF)-α activation of mesenchymal stromal cells (MSC) enhances their tumour-suppressive properties and tumour-homing ability. The molecular actors involved are unknown. We found that TNF induced MSC migration and tubulogenesis which correlated with a dose-dependent increase in Cavin-1 and Cavin-3 transcript levels. TNF triggered cyclooxygenase (COX)-2 expression, whereas specific siRNA-mediated gene silencing of Cavin-2 resulted in an amplified COX-2 expression, tubulogenesis, and migratory response partially due to a rapid and sustained increase in NF-κB phosphorylation status. Our results highlight a suppressive role for the caveolar component Cavin-2 in the angiogenic and inflammatory regulation of TNF-activated MSC.
Keywords : Mesenchymal stromal cells, Cavin, TNF, Cancer, Angiogenesis, Inflammation

November 2016, 9 (2)