Etiology and PathogenesisInvasion


Journal of Neuro-Oncology, 71(2): 99-106, January 2005. (Laboratory Investigation)


Abstract

Ganglioside GM3 inhibits proliferation and invasion of glioma

Yasunori Fujimoto, Shuichi Izumoto, Tsuyoshi Suzuki, Manabu Kinoshita, Naoki Kagawa, Kouichi Wada, Naoya Hashimoto, Motohiko Maruno, Yuji Nakatsuji and Toshiki Yoshimine

Department of Neurosurgery, Osaka University Medical School, Suita, Osaka, Japan [Y.F., S.I., T.S., M.K., N.K. K.W. N.H., M.M., T.Y.]. Department of Neurology, Osaka University Medical School, Suita,Osaka, Japan [Y.N.]. Department of Neurosurgery, Osaka University Medical School, E6 2-2 Yamadaoka, Suita, Osaka 565-0871, Japan [S.I.]. 
Correspondence to: Shuichi Izumoto, Email: sizumoto@nsurg.med.osaka-u.ac.jp, Phone: +81-6-6879-3652, Fax: +81-6-6879-3659

GM3, the simplest ganglioside, modulates cell adhesion, proliferation and differentiation in the central nervous system and exogenously added GM3 regulates cell–cell and cell–extracellular matrix adhesion and induces apoptosis. 
To assess the anti-tumor action of exogenous GM3, we examined its effect on the proliferation and invasion of glioma cells. 
Its inhibitory effect on cell proliferation was demonstrated in vitro by 3-(4,5-dimethyl-2-thiazol-2-yl) 2,5-diphenyltetrazolium bromide (MTT) assay and in vivo in rats with meningeal gliomatosis whose survival was significantly prolonged by the intrathecal injection of GM3. 
Terminal deoxynucleotidyl transferase-mediated dUTP-biotin nick end-labeling (TUNEL) assay revealed that GM3 induced glioma cell apoptosis in vitro and in vivo. In rat brain slice cultures, GM3 suppressed the invasion of glioma cells; this effect manifested earlier than the inhibition of cell proliferation and before apoptosis induction. 
Our results suggest exogenous GM3 as a potential therapeutic agent in patients with glioma requiring adjuvant therapy.

Keywords  apoptosis - brain slice culture - ganglioside - glioma - GM3 - invasion

© Springer 2005

Source: http://www.springerlink.com/openurl.asp?genre=article&eissn=1573-7373&volume=71&issue=2&spage=99
DOI: http://dx.doi.org/10.1007/s11060-004-9602-3


 

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