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Glycobiology Advance Access published online on May 4, 2005
Glycobiology, doi:10.1093/glycob/cwi071
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© The Author 2005. Published by Oxford University Press. All rights reserved. For permissions, please e-mail: journals.permissions@oupjournals.org
Received March 15, 2005
Revised April 26, 2005
Accepted April 27, 2005

Article

Polysialic acid facilitates tumor invasion by glioma cells

Masami Suzuki 1, Misa Suzuki 2, Jun Nakayama 3, Atsushi Suzuki 4, Kiyohiko Angata 5, Shihao Chen 5, Keiichi Sakai 6, Kazuki Hagihara 7, Yu Yamaguchi 7, and Minoru Fukuda 5*

1 Glycobiology, Cancer Research Center, The Burnham Institute, La Jolla, CA 92037; These authors equally contributed to this work; Present Address: Department of Obstetrics and Gynecology, Keio University School of Medicine, Tokyo 160-8582, Japan
2 Glycobiology, Cancer Research Center, The Burnham Institute, La Jolla, CA 92037; These authors equally contributed to this work
3 Department of Pathology, Shinshu University School of Medicine, Matsumoto 390-8621, Japan; These authors equally contributed to this work
4 Glycobiology, Cancer Research Center, The Burnham Institute, La Jolla, CA 92037; Present Address: Department of Obstetrics and Gynecology, Keio University School of Medicine, Tokyo 160-8582, Japan
5 Glycobiology, Cancer Research Center, The Burnham Institute, La Jolla, CA 92037
6 Department of Neurosurgery, Shinshu University School of Medicine, Matsumoto 390-8621, Japan
7 Developmental Neurobiology Programs, Cancer Research Center, The Burnham Institute, La Jolla, CA 92037

* To whom correspondence should be addressed.
Minoru Fukuda, E-mail: minoru{at}burnham.org


  Abstract

Polysialic acid is thought to attenuate NCAM adhesion, thereby facilitating neural cell migration and regeneration. Although the expression of polysialic acid has been shown to correlate with the progression of certain tumors such as small cell lung carcinoma, there have been no studies to determine the roles of polysialic acid in gliomas, the most common type of primary brain tumor in humans. In the present study, we first revealed that among patients with glioma, polysialic acid was detected more frequently in diffuse astrocytoma cells, which spread extensively. To determine directly the role of polysialic acid in glioma cell invasion, C6 glioma cells were transfected with polysialyltransferases to express polysialic acid. In those transfected cells polysialic acid is attached mainly to NCAM-140, while the mock-transfected C6 cells express equivalent amounts of polysialic acid-free NCAM-140. Both polysialic acid-negative and -positive C6 cell lines exhibited almost identical growth rates measured in vitro. However, polysialic acid-positive C6 cells exhibited increased invasion to the corpus callosum where the mock-transfected C6 glioma cells rarely invaded when inoculated into the brain. By contrast, the invasion to the corpus callosum by both the mock-transfected and polysialic acid-positive C6 cells was observed in NCAM-deficient mice. These results combined indicate that polysialic acid facilitates tumor invasion of glioma in the brain, and that NCAM-NCAM interaction is likely attenuated in the polysialic acid-mediated tumor invasion.

Keywords: Polysialic acid/glioma/tumor invasion/NCAM/polysialyltransferases.
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