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Glycobiology Advance Access published online on May 18, 2009
Glycobiology, doi:10.1093/glycob/cwp064
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© The Author 2009. Published by Oxford University Press. All rights reserved. For permissions, please e-mail: journals.permissions@oxfordjournals.org

Size dependent regulation of Snail2 by hyaluronan: its role in cellular invasion

Evisabel A. Craig1, Patti Parker1 and Todd D. Camenisch1,23

1 Department of Pharmacology and Toxicology
2 Steele Children's Research Center and Bio5 Institute, The University of Arizona, Tucson, Arizona 85721

3 To whom correspondence should be addressed: Department of Pharmacology and Toxicology, College of Pharmacy, The University of Arizona, Tucson, AZ 85721. Tel.: 520-626-0240; fax: 520-626-2466; e-mail: camenisch{at}pharmacy.arizona.edu.

Received on January 28, 2009; accepted on May 6, 2009

Hyaluronan (HA) induces changes in cellular behavior that are crucial during both embryonic development and cancer progression. However, the biological effects of varying sizes of HA and the signal transduction mechanisms that these polymers may activate remain unclear. In this study, we demonstrate that pulse stimulation of mouse embryonic fibroblasts with high molecular weight (HMW) HA, but not HA of lower molecular sizes, leads to increases in Snail2 protein which are dependent on NF{kappa}B activity. Involvement of CD44, the main HA receptor, in these responses was determined by use of a CD44 blocking antibody and CD44 siRNA. Both the blockade and silencing of CD44 significantly abrogate the increases in NF{kappa}B activity and Snail2 protein following HMW-HA stimulation. Furthermore, we show that HMW-HA induces cellular invasion and that inhibition of CD44, Snail2 or NF{kappa}B significantly decreases this response. These studies elucidate a novel HA/Snail2 functional connection through CD44 and NF{kappa}B that is important for the induction of cellular invasion and is dependent on HA size.

Key words: CD44 / cellular invasion / hyaluronan / NF{kappa}B / Snail2


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