Galectin-1 Pro-Angiogenic and
Pro-Migratory Effects in the Hs683 Oligodendroglioma Model Are Partly
Mediated Through the Control of BEX2 Expression
Le
Mercier M, Fortin S, Mathieu V, Roland I, Spiegl-Kreinecker S,
Haibe-KainS B, Bontempi G, Decaestecker C, Berger W, Lefranc F and Kiss
R
We
have previously reported that galectin-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, neo-angiogenesis and
migration. Down-regulating galectin-1 expression in Hs683 cells through
targeted siRNA 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.