Literature DB >> 18804092

Induction of follistatin precedes gastric transformation in gastrin deficient mice.

Weiqun Kang1, Milena Saqui-Salces, Yana Zavros, Juanita L Merchant.   

Abstract

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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Year:  2008        PMID： 18804092      PMCID： PMC2577233          DOI： 10.1016/j.bbrc.2008.09.031

Source DB:  PubMed          Journal:  Biochem Biophys Res Commun        ISSN： 0006-291X            Impact factor:   3.575


  25 in total

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  9 in total

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Review 6.  Recapitulating Human Gastric Cancer Pathogenesis: Experimental Models of Gastric Cancer.

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9.  Inflammation and Gli2 suppress gastrin gene expression in a murine model of antral hyperplasia.

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  9 in total

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