Published 21 June 2004. doi:10.1083/jcb1656iti5
The Rockefeller University Press, 0021-9525 $8.00
JCB, Volume 165, Number 6, 755-755
Tumors make do with less matrix
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MCSP (green) colocalizes with  4 integrin (red) as it amplifies the pathway activation seen during adhesion.
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Cell growth is controlled, in part, by the extracellular matrix and the intracellular signals that it elicits. No matrix usually means no growth. But, as reported by Yang et al. (page 881), some cancerous cells can probably get by with very little matrix by making their own costimulator.
That costimulator is melanoma chondroitin sulfate proteoglycan (MCSP). MCSP is known to be an early cell surface marker during melanoma progression, and to stimulate tumorigenesis. When Yang et al. transfected MCSP into a melanoma cell lacking MCSP, the cells exhibited an increased propensity to undergo spreading, which was mediated in large part by focal adhesion kinase (FAK). Integrin-mediated activation of both FAK and ERK 1/2 were increased by MCSP expression, and activation of ERK 1/2 remained even when FAK activity was inhibited.
MCSP is up-regulated early in melanoma (even in precancerous lesions), and its expression is maintained in the vast majority of melanomas throughout progression. The authors speculate that MCSP may function to lessen the requirement by tumor cells for ligands in the tumor microenvironment, giving cells that express this cell surface proteoglycan a selective advantage. 
Aparna Sreenivasan
aparnas{at}nasw.org
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