在胃泌素缺乏的小鼠中，卵泡抑素的诱导先于胃的转变。
Induction of follistatin precedes gastric transformation in gastrin deficient mice.
作者信息
Kang Weiqun, Saqui-Salces Milena, Zavros Yana, Merchant Juanita L
机构信息
Department of Internal Medicine, University of Michigan, 109 Zina Pitcher Place, BSRB 2051, Ann Arbor, MI 48109-2200, USA.
出版信息
Biochem Biophys Res Commun. 2008 Nov 21;376(3):573-7. doi: 10.1016/j.bbrc.2008.09.031. Epub 2008 Sep 17.
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.
我们之前表明，胃泌素缺陷（Gas(-/-)）小鼠会发生胃窦肿瘤。因此，对Gas(-/-)小鼠进行了为期12个月的连续研究，以确定胃转变潜在的分子机制。Gas(-/-)小鼠在9个月时出现胃底萎缩。胃窦黏膜增生与TFF1和Muc5AC的局灶性缺失同时出现。对12个月大的Gas(-/-)肿瘤进行微阵列分析，发现卵泡抑素增加，卵泡抑素是一种激活素/BMP拮抗剂。我们发现，卵泡抑素表达升高发生在增生性胃窦的增殖颈部区域、Gas(-/-)小鼠的胃窦肿瘤以及人类胃癌中。卵泡抑素在一种胃癌细胞系中诱导细胞周期蛋白D1以及三叶因子TFF1和TFF2。我们得出结论，Gas(-/-)小鼠的胃窦增生涉及由于卵泡抑素导致的黏液细胞谱系扩增，提示其在胃窦肿瘤发生中的作用。
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