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Fig. 4 | Journal of Experimental & Clinical Cancer Research

Fig. 4

From: Diabetes promotes invasive pancreatic cancer by increasing systemic and tumour carbonyl stress in KrasG12D/+ mice

Fig. 4

Association between AGE levels (carbonyl stress burden), ERK 1/2 phosphorilation status and YAP activation in murine and human PaC. Representative Western blots for AGEs (a), phosphorylated and total ERK 1/2 (b), CTGF (c) and nuclear YAP (d) in control (Ctr), diabetic (Diab), and Diab treated with FL-926-16 (Diab+FL) KCM mice at the time of sacrifice and relative band densitometry analysis from five mice per group. Each dot represents one case and bars represent mean ± SEM. Dual-label immunofluorescence (d) for AGEs (red) and YAP (green). DAPI (blue): 4′,6-diamidino-2-phenylindole. Original magnification: 250X, scale bar: 200 μm. Active (non-phosphorylated) YAP immunohistochemistry staining (e, upper panels, original magnification: 400X, scale bar: 200 μm) in representative low and high carbonyl stress human pancreatic adenocarcinomas as assessed by their AGE level (e, lower panels, original magnification: 250X, scale bar: 200 μm). Linear regression analysis (f) of the correlation between the ratio of YAP-positive nuclei to total nuclei with percentage of tumour tissue positive for AGE staining (n = 14). Red dots = patients with a clinical diagnosis of diabetes mellitus prior to undergoing surgery; black dots = non-diabetic subjects. Post hoc multiple comparison: ***P < 0.001 vs Ctr; †††P < 0.001 or ††P < 0.01 vs Diab

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