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. 2016 Feb 8;7(10):11349–11363. doi: 10.18632/oncotarget.7239

Figure 5. HNF4α and IL-1R1 is essential for IL-1β-induced expression and phosphorylation of p65.

Figure 5

A. and B. Western blot shows pre-treatment with HNF4α siRNA in AGS and BGC-823 cells decreased p65 expression and phosphorylation induced by IL-1β(10ng/ml). Foci formation assay showed knock down of HNF4α attenuates the pro-foci formation effect of IL-1β in AGS and BGC-823 cells. *p<0.05,**p<0.01 by Student's t-test. C. Western blot and foci formation assay shows HNF4α over-expression markedly increased p65 phosphorylation and foci formation induced by IL-1β in GES-1 cell lines. D. Western blot sand foci formation assay shows HNF4α over-expression in GES-1 cells retrieved IL-1β transduction when IL-1R1 was blockaded by IL-1RA (500ng/ml). E. p65, HNF4α, IL-1R1, and ki67 expression in serial sections from atrophic gastritis and gastric cancer. Representative images are shown here (magnification 400x;Scale bars:50μm). F. Schematic representation of the proposed HNF4α and IL-1R1 feedback circuit in Hp associated gastric oncogenesis.