Fig. 4: Loss of either DUSP5 or DUSP6 promotes changes in ERK activation and SOX9 expression during KRASG12D-driven pancreatic carcinogenesis. | Oncogene

Fig. 4: Loss of either DUSP5 or DUSP6 promotes changes in ERK activation and SOX9 expression during KRASG12D-driven pancreatic carcinogenesis.

From: Suppression of mutant Kirsten-RAS (KRASG12D)-driven pancreatic carcinogenesis by dual-specificity MAP kinase phosphatases 5 and 6

Fig. 4: Loss of either DUSP5 or DUSP6 promotes changes in ERK activation and SOX9 expression during KRASG12D-driven pancreatic carcinogenesis.The alternative text for this image may have been generated using AI.

Immunohistochemical analysis of 56-day age-matched pancreata of the indicated cohorts. Cohorts consisted of the following genotypes: KrasLSL-G12D/+; Ptf1a-Cre; Dusp+/+ (KC), KrasLSL-G12D/+; Ptf1a-Cre; Dusp5+/fl (KCD5+/−), KrasLSL-G12D/+; Ptf1a-Cre; Dusp5fl/fl (KCD5−/−), KrasLSL-G12D/+; Ptf1a-Cre; Dusp6+/fl (KCD6+/−) and KrasLSL-G12D/+; Ptf1a-Cre; Dusp6fl/fl (KCD6−/−). Representative images (A) and H-score quantification (B) of staining for p-ERK1/2 in PanINs of the indicated cohorts. Representative images (C) and H-score quantification (D) of staining for p-ERK1/2 and SOX9 in the acinar tissue of the indicated cohorts. (Scale bars, 200 µm.) Quantification was performed on one representative section per mouse, individual data points and mean are shown, n = 7 mice per cohort. N nuclear, C cytoplasmic, ns not significant, *p < 0.05, **p < 0.01, using one-way ANOVA and Bonferroni post hoc test.

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