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Int J Stem Cells. 2017 May 30;10(1):103-113. doi: 10.15283/ijsc16032.

Cavin-2 Functions as a Suppressive Regulator in TNF-induced Mesenchymal Stromal Cell Inflammation and Angiogenic Phenotypes.

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Laboratoire d'Oncologie Moléculaire, Département de Chimie, Centre de recherche BIOMED, Université du Québec à Montréal, Quebec, Canada.
Département de Physiologie Moléculaire et Intégrative, Faculté de Médecine, Université de Montréal, Montreal, Canada.


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.


Angiogenesis; Cancer; Cavin; Inflammation; Mesenchymal stromal cells; TNF

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