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Biochem Biophys Res Commun. 2008 Nov 21;376(3):573-7. doi: 10.1016/j.bbrc.2008.09.031. Epub 2008 Sep 17.

Induction of follistatin precedes gastric transformation in gastrin deficient mice.

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  • 1Department of Internal Medicine, University of Michigan, 109 Zina Pitcher Place, BSRB 2051, Ann Arbor, MI 48109-2200, USA.


We previously showed that antral gastric tumors develop in gastrin-deficient (Gas(-/-)) mice. Therefore Gas(-/-) mice were studied sequentially over 12 months to identify molecular mechanisms underlying gastric transformation. Fundic atrophy developed by 9 months in Gas(-/-) mice. Antral mucosal hyperplasia developed coincident with the focal loss of TFF1 and Muc5AC. Microarray analysis of 12 month Gas(-/-) tumors revealed an increase in follistatin, an activin/BMP antagonist. We found that elevated follistatin expression occurred in the proliferative neck zone of hyperplastic antrums, in antral tumors of Gas(-/-) mice, and also in human gastric cancers. Follistatin induced cyclin D1 and the trefoil factors TFF1 and TFF2 in a gastric cancer cell line. We concluded that antral hyperplasia in Gas(-/-) mice involves amplification of mucous cell lineages due to follistatin, suggesting its role in the development of antral gastric tumors.

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