Sfrp1 Loss Accelerates Tumor Initiation and SCC Progression
(A) Schematic representation for two-step chemical-induced carcinogenesis using DMBA/TPA.
(B) WT, Sfrp1+/−, and Sfrp1−/− mice showing difference in tumor formation after 12 weeks of TPA application. Red arrows show papilloma formation in Sfrp1−/− mice.
(C) WT, Sfrp1+/−, and Sfrp1−/− mice showing difference in tumor formation after 18 weeks of TPA application. Yellow circles show papilloma formation in Sfrp1+/− and Sfrp1−/− mice.
(D) WT, Sfrp1+/−, and Sfrp1−/− mice showing difference in tumor formation after 25 weeks of TPA application.
(E) Graph depicting percentage of papilloma incidence versus TPA application in weeks, in WT, Sfrp1+/−, and Sfrp1−/−, mice (n = 11 mice/genotype).
(F) Graph depicting average number of tumors per mouse in WT, Sfrp1+/−, and Sfrp1−/− mice (n = 17 for WT, n = 10 for Sfrp1+/−, and n = 19 for Sfrp1−/−).
WT, wild type; Sfrp1+/−, heterozygous for Sfrp1; Sfrp1−/−, homozygous knockout for Sfrp1; DMBA, 7,12-dimethylbenz[a]anthracene; TPA, 12-O-tetradecanoyl phorbol-13-acetate; A, anagen; C, catagen; T, telogen; M, morphogenesis; SCC, squamous cell carcinoma. Data were analyzed by Student's t test and presented as means ± SEM. ∗∗p < 0.01, ∗∗∗p < 0.001. See also Figure S1.