What lurks beneath: IL-11, via Stat3, promotes inflammation-associated gastric tumorigenesis

Research output: Contribution to journalComment/debatepeer-review

22 Scopus citations

Abstract

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-β 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-β family, that originate from the stroma.

Original languageEnglish (US)
Pages (from-to)1628-1631
Number of pages4
JournalJournal of Clinical Investigation
Volume118
Issue number5
DOIs
StatePublished - May 1 2008
Externally publishedYes

ASJC Scopus subject areas

  • General Medicine

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