Induction of follistatin precedes gastric transformation in gastrin deficient mice

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

doi:10.1016/j.bbrc.2008.09.031

Induction of follistatin precedes gastric transformation in gastrin deficient mice

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

Research output: Contribution to journal › Article › peer-review

14 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 language	English (US)
Pages (from-to)	573-577
Number of pages	5
Journal	Biochemical and Biophysical Research Communications
Volume	376
Issue number	3
DOIs	https://doi.org/10.1016/j.bbrc.2008.09.031
State	Published - Nov 21 2008
Externally published	Yes

Keywords

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

ASJC Scopus subject areas

Biophysics
Biochemistry
Molecular Biology
Cell Biology

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10.1016/j.bbrc.2008.09.031

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title = "Induction of follistatin precedes gastric transformation in gastrin deficient mice",

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.",

keywords = "Activins, Atrophic gastritis, Follistatin, Gastric cancer, Gastrin, Intestinal metaplasia, Muc6, Mucous neck cell, TFF1",

author = "Weiqun Kang and Milena Saqui-Salces and Yana Zavros and Merchant, {Juanita L.}",

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.",

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doi = "10.1016/j.bbrc.2008.09.031",

language = "English (US)",

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T1 - Induction of follistatin precedes gastric transformation in gastrin deficient mice

AU - Kang, Weiqun

AU - Saqui-Salces, Milena

AU - Zavros, Yana

AU - Merchant, Juanita L.

N1 - 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.

PY - 2008/11/21

Y1 - 2008/11/21

N2 - 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.

AB - 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.

KW - Activins

KW - Atrophic gastritis

KW - Follistatin

KW - Gastric cancer

KW - Gastrin

KW - Intestinal metaplasia

KW - Muc6

KW - Mucous neck cell

KW - TFF1

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JO - Biochemical and Biophysical Research Communications

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Induction of follistatin precedes gastric transformation in gastrin deficient mice

Abstract

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