Back to Search Start Over

Selective osteopontin knockdown exerts anti-tumoral activity in a human glioblastoma model.

Authors :
Lamour, Virginie
Le Mercier, Marie
Lefranc, Florence
Hagedorn, Martin
Javerzat, Sophie
Bikfalvi, Andreas
Kiss, Robert
Castronovo, Vincent
Bellahcene, Akeila
Lamour, Virginie
Le Mercier, Marie
Lefranc, Florence
Hagedorn, Martin
Javerzat, Sophie
Bikfalvi, Andreas
Kiss, Robert
Castronovo, Vincent
Bellahcene, Akeila
Source :
International journal of cancer, 126 (8
Publication Year :
2010

Abstract

Osteopontin (OPN), a member of the SIBLING (Small Integrin-Binding LIgand N-linked Glycoprotein) family, is overexpressed in human glioblastoma. Higher levels of OPN expression correlate with increased tumor grade and enhanced migratory capacity of tumor cells. Based on these observations, we explored the possibility that knocking down OPN expression in glioblastoma cells could exert an anti-tumoral activity using an avian in vivo glioblastoma model that mimics closely human gliobastoma. Human U87-MG glioma cells transfected with specific anti-OPN small interfering RNAs (siRNAs) were grafted onto the chicken chorio-allantoic membrane (CAM). OPN-deficient U87-MG cells gave rise to tumors that were significantly smaller than tumors formed from untransfected cells (paired t-test, p < 0.05). Accordingly, the amount of proliferating cells in OPN-deficient tumors showed a six-fold reduction when compared to control tumors. However, OPN inhibition did not affect significantly tumor-associated angiogenesis. In vitro, OPN-silenced U87-MG and U373-MG cells showed decreased motility and migration. This is the first demonstration that OPN inhibition blocks glioma tumor growth, making this invasion-related protein an attractive target for glioma therapy.<br />JOURNAL ARTICLE<br />SCOPUS: ar.j<br />FLWIN<br />info:eu-repo/semantics/published

Details

Database :
OAIster
Journal :
International journal of cancer, 126 (8
Notes :
1 full-text file(s): application/pdf, English
Publication Type :
Electronic Resource
Accession number :
edsoai.on1363712076
Document Type :
Electronic Resource