Glycogen Synthase Kinase-3beta regulates Snail and beta-catenin during gastrin-induced migration of gastric cancer cells.

Journal of Molecular Signaling
Prajna MishraBasabi Rana

Abstract

The gastrointestinal peptide hormone gastrin is known to regulate various cellular processes including proliferation, migration and metastasis in gastrointestinal (GI) cells. The studies described here were undertaken to elucidate in detail the signaling pathways mediating the migratory responses of amidated gastrin (G17) and to understand the involvement of the serine/threonine kinase Glycogen Synthase Kinase-3 beta (GSK3beta) in this. Our results indicate that incubation of gastric cancer cells overexpressing CCK2 receptor (AGSE cells) with G17 results in a dose and time dependent increase of GSK3betaSer9 phosphorylation, indicative of an inhibition of the kinase. Pretreatment with a pharmacological inhibitor of PI3Kinase pathway (Wortmannin) was unable to antagonize G17-induced GSK3betaSer9 phosphorylation, suggesting that this might involve PI3Kinase-independent pathways. Treatment with G17 was also associated with increased Snail expression, and beta-catenin nuclear translocation, both of which are GSK3beta downstream targets. Pretreatment with a pharmacological inhibitor of GSK3beta (AR-A014418) augmented Snail expression and beta-catenin nuclear translocation in the absence of G17, whereas overexpression of a phosphoryla...Continue Reading

Citations

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Methods Mentioned

BETA
nuclear translocation
transfection

Software Mentioned

Axiovision

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