Fig. 5. Oncogenic Ras tumor regression following deletion of C/EBPβ is dependent on p53.

a Schematic of the K14-CreER^tam;C/EBPβ^flox/flox;p53^flox/flox (DIKO) transgenic mouse model system. b Western blot analysis of C/EBPβ and p53 in epidermal lysates of tamoxifen-treated Cre, IKOβ, IKOp53, and DIKO mice. c IHC staining for C/EBPβ and p53 in normal DIKO mouse skin following vehicle and tamoxifen treatment. D dermis, E epidermis. Scale bar: 10 μm. d H&E and IHC staining for C/EBPβ and p53 in DMBA/TPA-induced mouse squamous papillomas following tamoxifen dosing. e Tumor multiplicity in DMBA/TPA-induced skin squamous papilloma in Cre and DIKO mice dosed with tamoxifen at 19 weeks of skin tumor promotion (Cre N = 10 mice, DIKO N = 11 mice). f Tumor incidence in Cre and DIKO mice. g Tumor volume in Cre and DIKO mice. h Tumor multiplicity in Cre, IKOβ, IKOp53, and DIKO mice before and after tamoxifen collected 2 weeks after initial tamoxifen dose (Cre N = 5 mice, IKOβ N = 3 mice, IKOp53 N = 5 mice, DIKO N = 5 mice). # indicates IKOβ is significantly different from Cre p < 0.05 via the Student’s t-test. i Quantification of γH2AX IHC staining (Cre n = 9 tumors, IKOβ n = 3 tumors, IKOp53 n = 7 tumors, DIKO n = 7 tumors). j Quantification of apoptosis in H&E-stained tumors collected 2 weeks after the initial tamoxifen dose (Cre n = 9 tumors, IKOβ n = 3 tumors, IKOp53 n = 7 tumors, DIKO n = 7 tumors). Data are expressed as mean ± SD. *Significantly different from controls p < 0.05 via the Student’s t-test