Fig. 2
Keap1 inactivation accelerates KrasG12D-induced lung adenocarcinoma. a Survival analysis of K (n = 10) and KK (n = 19) mice following Ad5-CMV-Cre administration. Mantel-Cox test: ****p < 0.0001. b Hematoxylin and eosin (H&E) stained lungs of representative K and KK mice at ethical endpoint. Scale, 1 mm; inset, 100 μm. c Weight of left lung lobe of uninfected littermates (U, n = 8), K (n = 5) and KK (n = 14) mice 3 months following Ad5-CMV-Cre infection. Ordinary one-way ANOVA/Holm-Sidak’s multiple comparisons test: U v K: **p = 0.006; U v KK: ****p < 0.0001; K v KK: *p = 0.0327. Mean ± SEM. d Number of lesions in the lungs of K (n = 4) and KK (n = 7) mice 3 months post Ad5-CMV-Cre. Ordinary one-way ANOVA/Tukey’s multiple comparisons test K v KK *p = 0.0397. Mean ± SEM. e Lesion classification of K (n = 4) and KK (n = 7) lungs 3 months post Ad5-CMV-Cre infection. Two-way ANOVA/Tukey’s multiple comparisons test: alveolar hyperplasia K v KK *p = 0.05, adenoma K v KK *p = 0.05. Mean ± SEM. f Immunofluorescence of EYFP and Nrf2 expression in EYFPT/+;KrasG12D/+;Keap1Δ/Δ three months following Ad5-CMV-Cre infection. Boxes represent EYFP positive and negative regions. Scale, 10 μm. g Quantification of 2,7-dichlorofluorescin diacetate (DCFDA) alone or in combination with 110 μM tert-butyl hydrogen peroxide (TBHP) to stimulate reactive oxygen species (ROS) in primary cell lines (n = 4 KP and KK). Mann–Whitney test DCFDA + TBHP KP v KK *p = 0.0286. Mean ± SEM
