Fig. 7: Negative expression of ITF2 and p65 in CAC tissues.
From: Protein stabilization of ITF2 by NF-κB prevents colitis-associated cancer development
A Representative immuno-stained images of ITF2, β-catenin, and p65 in normal, dysplasia, and carcinoma CAC tissues. The data are representative of three independent experiments. B Nuclear-positive expression levels of ITF2, β-catenin, and p65 were counted and analyzed in CAC specimens. C The GEO dataset (GSE3629) was analyzed for ITF2 gene expression in UC-NonCa (43 patients), UC-Ca (10 patients), sporadic Ca (60 patients), and UC-associated Ca (6 patients). The heat-map image was generated using the Multiple Experiment Viewer (MEV) software. The color scale represents relative expression values; blue, low expression score; red, high expression score. D Graphical summary of ITF2 regulation by p65. Schematic illustrations were generated with BioRender (BioRender.com). Normally, ITF2 is ubiquitinated by a Parkin, leading to ubiquitination and proteasomal degradation of ITF2. In inflammatory conditions, such as dysplasia, where p65 is increased, p65 levels are upregulated, leading to ITF2 protein stabilization, thereby interrupting p65 activation. In carcinoma, p65 is further activated owing to ITF2 loss and leads to excessive expression of pro-tumorigenic cytokines such as IL-6, TNF, IL-8, and IL-1β, thereby contributing to eventual CAC development. Scale bars, 100 μm. All results are presented as means ± SEM. Statistical significance was determined by Kruskal–Wallis tests followed by the two-tailed Mann–Whitney U test (B, **P < 0.0001) for pairwise comparisons. Source data are provided in the Source Data file.
