Galectin-1 modulates human glioblastoma cell migration into the brain through modifications to the actin cytoskeleton and levels of expression of small GTPases

Isabelle Camby; Nathalie Belot; Florence Lefranc; Niloufar Sadeghi; Yvan de Launoit; Herbert Kaltner; Sophie Musette; Francis Darro; André Danguy; Isabelle Salmon; Hans-Joachim Gabius; Robert Kiss

doi:10.1093/jnen/61.7.585

Galectin-1 modulates human glioblastoma cell migration into the brain through modifications to the actin cytoskeleton and levels of expression of small GTPases

J Neuropathol Exp Neurol. 2002 Jul;61(7):585-96. doi: 10.1093/jnen/61.7.585.

Authors

Isabelle Camby¹, Nathalie Belot, Florence Lefranc, Niloufar Sadeghi, Yvan de Launoit, Herbert Kaltner, Sophie Musette, Francis Darro, André Danguy, Isabelle Salmon, Hans-Joachim Gabius, Robert Kiss

Affiliation

¹ Laboratory Histopathology, Faculty of Medicine, Erasmus University Hospital, Université Libre de Bruxelles, Brussels, Belgium.

PMID: 12125737
DOI: 10.1093/jnen/61.7.585

Abstract

We show that high-grade astrocytic tumors with high levels of galectin-1 expression are associated with dismal prognoses. The immunohistochemical analysis of galectin-1 expression of human U87 and U373 glioblastoma xenografts from the brains of nude mice revealed a higher level of galectin-1 expression in invasive areas rather than non-invasive areas of the xenografts. Nude mice intracranially grafted with U87 or U373 cells constitutively expressing low levels of galectin-1 (by stable transfection of an expression vector containing the antisense mRNA of galectin-1) had longer survival periods than those grafted with U87 or U373 cells expressing normal levels of galectin-1. Galectin-1 added to the culture media markedly and specifically increased cell motility levels in human neoplastic astrocytes. These effects are related to marked modifications in the organization of the actin cytoskeleton and the increase in small GTPase RhoA expression. All the data obtained indicate that galectin-1 enhances the migratory capabilities of tumor astrocytes and, therefore, their biological aggressiveness.

Publication types

Research Support, Non-U.S. Gov't

MeSH terms

Actin Cytoskeleton / drug effects
Actin Cytoskeleton / metabolism*
Actin Cytoskeleton / pathology
Animals
Brain / metabolism
Brain / pathology
Brain / surgery
Brain Neoplasms / metabolism*
Brain Neoplasms / pathology
Brain Neoplasms / physiopathology
Brain Tissue Transplantation
Cell Movement / drug effects
Cell Movement / physiology*
Disease Progression
Female
Galectin 1
Gene Expression Regulation, Neoplastic / drug effects
Gene Expression Regulation, Neoplastic / physiology
Glioblastoma / metabolism*
Glioblastoma / pathology
Glioblastoma / physiopathology
Graft Survival / drug effects
Graft Survival / physiology
Hemagglutinins / genetics
Hemagglutinins / metabolism*
Hemagglutinins / pharmacology
Humans
Male
Mice
Mice, Nude
Neoplasm Invasiveness / pathology
Neoplasm Invasiveness / physiopathology*
RNA, Antisense / genetics
Survival Rate
Tumor Cells, Cultured / drug effects
Tumor Cells, Cultured / metabolism*
Tumor Cells, Cultured / transplantation
rhoA GTP-Binding Protein / drug effects
rhoA GTP-Binding Protein / metabolism*

Substances

Galectin 1
Hemagglutinins
RNA, Antisense
rhoA GTP-Binding Protein