Fig. 3: EGFR pathway is the intermediary agent for SPINK4 participating in GC differentiation.
From: Therapeutic potential of the secreted Kazal-type serine protease inhibitor SPINK4 in colitis
a Relative expression of IEC markers from different branches, including enteroendocrine cells (Neurog3, Insm, and Pax4), secretory lineage (Muc2, Gfi1, Foxa2, Reg3a, and Lyz), M cells (Spib), Tuft cells (Dclk), stem cells (Olfm4, Lgr5), and absorptive cells (Si) in mouse organoids with rSPINK4 stimulation. The degree of color depth indicates the abundance of expression positively. b Levels of phosphorylated and total EGFR in NCM460 and HT-29 cells with 5 ng/mL rSPINK4 stimulation for 0–60 min. c Direct downstream molecules of the EGFR pathway detected using western blotting with rSPINK4 stimulation for 0–60 min. d Typical fluorescent images of intestinal organoids from WT and KO mice including MUC2 (green), E-cadherin (red), and DAPI (blue), with rSPINK4 (100 ng/mL) and AG1478 (10 μM) stimulation under inflammatory conditions (50 ng/mL TNF-α treatment). e Quantitative analysis of weight loss with SPINK4 and gefitinib intervention following DSS administration in the control group drinking water (control, n = 4); DSS and PBS administration group (DSS + PBS, n = 6); DSS and rSPINK4 administration group (DSS + rSPINK4, n = 5); and DSS, rSPINK4, and gefitinib administration group (DSS + rSPINK4 + gefitinib, n = 4). f Representative canonical endoscopic images with the lesion circled with white arrows. g Quantification of colonic length. h The levels of the phosphorylated and total EGFR were determined in WT and KO mouse tissues (upper panel) and rSPINK4 treatment group (lower panel). Data are presented as the mean ± SEM. All tests were two-sided. Statistical significance was calculated using unpaired Student’s t test (h). Besides, Kruskal–Wallis test (h) and one-way ANOVA (b, e, g) were performed for multiple comparison; n = 3–5 biologically independent experiments (b, g, h). Source data are provided as a Source Data file.
