The gene for the axonal cell adhesion molecule TAX-1 is amplified and aberrantly expressed in malignant gliomas.

TitleThe gene for the axonal cell adhesion molecule TAX-1 is amplified and aberrantly expressed in malignant gliomas.
Publication TypeJournal Article
Year of Publication2001
AuthorsRickman DS, Tyagi R, Zhu XX, Bobek MP, Song S, Blaivas M, Misek DE, Israel MA, Kurnit DM, Ross DA, Kish PE, Hanash SM
JournalCancer Res
Volume61
Issue5
Pagination2162-8
Date Published2001 Mar 01
ISSN0008-5472
KeywordsBlotting, Northern, Brain Neoplasms, Cell Adhesion Molecules, Neuronal, Cell Movement, Contactin 2, Down-Regulation, Gene Amplification, Gene Expression Regulation, Neoplastic, Glioblastoma, Humans, Immunohistochemistry, Membrane Glycoproteins, Reverse Transcriptase Polymerase Chain Reaction, RNA, Messenger
Abstract

The human TAX-1 gene encodes a Mr 135,000 glycoprotein that is transiently expressed on the surface of a subset of neurons during development and is involved in neurite outgrowth. The TAX-1 gene has been mapped to a region on chromosome 1 that has been implicated in microcephaly and the Van der Woude syndrome. Using restriction landmark genome scanning to search for amplified genes in gliomas, we found TAX-1 to be amplified in 2 high-grade gliomas among a group of 26 gliomas investigated. Real-time reverse transcription-quantitative PCR analysis detected high levels of TAX-1 mRNA in glial tumors, even in the absence of TAX-1 gene amplification. Immunohistochemical analysis revealed abundant levels of TAX-1 in neoplastic glial cells of glioblastoma multiforme tumors. Because glial tumors are highly invasive and in view of the role of TAX-1 in neurite outgrowth, we investigated the potential role of TAX-1 in glioma cell migration. Using an in vitro assay, we found that the migration of glioma tumor cells is profoundly reduced in the presence of either an anti-TAX-1 antibody or a TAX-1 antisense oligonucleotide. Our findings suggest that TAX-1 plays a role in glial tumorigenesis and may provide a potential target for therapeutic intervention.

Alternate JournalCancer Res
PubMed ID11280781
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