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Galectin 1 Proangiogenic and Promigratory Effects in the Hs683 Oligodendroglioma Model Are Partly Mediated through the Control of BEX2 Expression1

By Marie Le Mercier, Shannon Fortin, Véronique Mathieu, Isabelle Roland, Sabine Spiegl-Kreinecker, Benjamin Haibe-Kains, Gianluca Bontempi, Christine Decaestecker, Walter Berger, Florence Lefranc and Robert Kiss

Abstract

We have previously reported that galectin 1 (Gal-1) plays important biological roles in astroglial as well as in oligodendroglial cancer cells. As an oligodendroglioma model, we make use of the Hs683 cell line that has been previously extensively characterized at cell biology, molecular biology, and genetic levels. Galectin 1 has been shown to be involved in Hs683 oligodendroglioma chemoresistance, neoangiogenesis, and migration. Down-regulating Gal-1 expression in Hs683 cells through targeted small interfering RNA provokes a marked decrease in the expression of the brain-expressed X-linked gene: BEX2. Accordingly, the potential role of BEX2 in Hs683 oligodendroglioma cell biology has been investigated. The data presented here reveal that decreasing BEX2 expression in Hs683 cells increases the survival of Hs683 orthotopic xenograft-bearing mice. Furthermore, this decrease in BEX2 expression impairs vasculogenic mimicry channel formation in vitro and angiogenesis in vivo, and modulates glioma cell adhesion and invasive features through the modification of several genes previously reported to play a role in cancer cell migration, including MAP2, plexin C1, SWAP70, and integrin β6. We thus conclude that BEX2 is implicated in oligodendroglioma biology

Topics: Research Articles
Publisher: Neoplasia Press Inc.
OAI identifier: oai:pubmedcentral.nih.gov:2671859
Provided by: PubMed Central
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