A Role for RUNX3 in Inflammation-Induced Expression of IL23A in Gastric Epithelial Cells
CagA
DOI:
10.1016/j.celrep.2014.06.003
Publication Date:
2014-07-05T20:15:16Z
AUTHORS (8)
ABSTRACT
RUNX3 functions as a tumor suppressor in the gastric epithelium, where its inactivation is frequently observed during carcinogenesis. We identified IL23A target gene epithelial cells. This was confirmed series of vitro analyses cell lines. In elucidating underlying regulatory network, we uncovered prominent role for TNF-α/NF-κB pathway activating transcription. Moreover, effect TNF-α markedly augmented by infection Helicobacter pylori, primary cause human gastritis. Of note, H. pylori utilized CagA/SHP2 to activate IL23A, well induction NOD1 iE-DAP. Importantly, synergized strongly with these physiologically relevant stimuli induce IL23A. Lastly, present evidence secretion cells form that distinct from canonical IL-23 (IL23A/IL12B).
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