What lurks beneath: IL-11, via Stat3, promotes inflammation-associated gastric tumorigenesis.
What lurks beneath: IL-11, via Stat3, promotes inflammation-associated gastric tumorigenesis.
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DOI：
10.1172/jci35344
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发表时间：
2008-05
期刊：
影响因子：
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通讯作者：
J. Merchant
中科院分区：
文献类型：
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作者：
J. Merchant
胃中的慢性炎症主要在远端胃或胃窦中诱导细胞转化和胃癌。在本期的JCI中，Ernst等人在小鼠中进行的一项研究为IL-11及其糖蛋白130（gp 130）受体在炎症相关胃上皮细胞致癌转化中的作用提供了新的见解，他们表明这是由Stat 3和Stat 1（在较小程度上）的活化增加介导并依赖于Stat 3和Stat 1的活化增加（参见1727页开始的相关文章）。该小组先前的研究表明，Stat 3过度活跃会刺激TGF-β抑制剂Smad 7。总的来说，这些研究表明，胃中致癌转化的一个重要途径是通过抑制生长抑制信号，如来源于基质的TGF-β家族成员。
Chronic inflammation in the stomach induces cellular transformation and gastric cancer primarily in the distal stomach or antrum. In this issue of the JCI, a study in mice by Ernst et al. provides new insight into the role of IL-11 and its glycoprotein 130 (gp130) receptor in inflammation-associated gastric epithelial cell oncogenic transformation, which they show is mediated by and dependent on increased activation of Stat3 and, to a lesser extent, Stat1 (see the related article beginning on page 1727). Prior studies from this group have shown that Stat3 hyperactivity stimulates the TGF-beta inhibitor Smad7. Collectively, the studies suggest that an important pathway of oncogenic transformation in the stomach is through suppression of growth inhibitory signals, such as members of the TGF-beta family, that originate from the stroma.