Journal
NEUROCHEMICAL RESEARCH
Volume 35, Issue 11, Pages 1796-1804Publisher
SPRINGER/PLENUM PUBLISHERS
DOI: 10.1007/s11064-010-0246-8
Keywords
Calcium; Calpain; Glioblastoma; Glutamate; Invasion; Matrix metalloproteinase
Categories
Funding
- Medical Research Foundation of Oregon
- Oregon State University
- National Institute of General Medical Sciences, National Institutes of Health [GM 63711]
- National Institute of Environmental Health Sciences, National Institutes of Health [P30 ES00210]
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Invasion of glioblastoma cells significantly reduces the effectiveness of current treatments, highlighting the importance of understanding dispersal mechanisms and characteristics of the invasive population. Induction of calcium fluxes into glioblastoma cells by autocrine glutamate is critical for invasion. However, the target(s) by which calcium acts to stimulate the dispersal of glioblastoma cells is not clear. In this study, we tested the hypothesis that the calcium-activated protease calpain 2 is required for glioblastoma cell invasion. Knockdown of calpain 2 expression using shRNA or chemical inhibition of calpain activity reduced glioblastoma cell invasion by 90%. Interestingly, decreased expression of calpain 2 did not influence morphology or migration, suggesting regulation of invasion specific mechanisms. Consistent with this idea, 39% less extracellular MMP2 was measured from knockdown cells identifying one mechanism by which calpain 2 mediates glioblastoma cell invasion. This is the first report demonstrating that calpain 2 is required for glioblastoma cell invasion.
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