Induction of follistatin precedes gastric transformation in gastrin deficient mice

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

Research output: Contribution to journalArticlepeer-review

10 Scopus citations

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.

Original languageEnglish (US)
Pages (from-to)573-577
Number of pages5
JournalBiochemical and Biophysical Research Communications
Volume376
Issue number3
DOIs
StatePublished - Nov 21 2008

Bibliographical note

Funding Information:
This work was supported in part by Public Health Service Grant R01-DK61410 to J.L.M. and the Michigan Gastrointestinal Peptide Research Center P30-DK34933.

Keywords

  • Activins
  • Atrophic gastritis
  • Follistatin
  • Gastric cancer
  • Gastrin
  • Intestinal metaplasia
  • Muc6
  • Mucous neck cell
  • TFF1

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