Induction of follistatin precedes gastric transformation in gastrin deficient mice
Induction of follistatin precedes gastric transformation in gastrin deficient mice
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DOI：
10.1016/j.bbrc.2008.09.031
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发表时间：
2008-11-21
影响因子：
3.1
通讯作者：
Merchant, Juanita L.
中科院分区：
文献类型：
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作者：
Kang, Weiqun;Saqui-Salces, Milena;Merchant, Juanita L.
我们之前发现胃胃窦肿瘤在胃泌素缺乏（Gas(-/-)）小鼠中发生。因此，对Gas（-/-）小鼠进行了为期12个月的连续研究，以确定胃转化的分子机制。Gas-/-小鼠在9个月后出现基底萎缩。胃窦粘膜增生与TFF1和Muc5AC的局灶性丧失同时发生。微阵列分析显示12个月的气体肿瘤中卵泡抑素（一种激活素/BMP拮抗剂）的含量增加。我们发现，在Gas（-/-）小鼠的窦腔肿瘤中，增生性窦腔的增生性颈部区出现了卵泡抑素的表达升高。在人类胃癌中也是如此。卵泡抑素诱导胃癌细胞周期蛋白D1和三叶因子TFF1、TFF2的表达。我们得出结论，Gas（-/-）小鼠的胃窦增生涉及由于卵泡抑素引起的粘膜细胞系扩增，提示其在胃窦肿瘤的发展中起作用。(c) 2008爱思唯尔公司版权所有。
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. (c) 2008 Elsevier Inc. All rights reserved.