Fig. 2: Gal-7 favors tumor growth in a murine skin carcinogenesis model.
From: Galectin-7 reprograms skin carcinogenesis by fostering innate immune evasive programs

Lgals7−/−, WT and Tg46 mice were subjected to a two-stage carcinogenesis protocol (DMBA/TPA). A Weekly monitoring of tumor growth. Tumor number in each experimental group (left panel; mean ± SEM of 4 independent experiments, each experiment with n = 5 mice per group) and representative images of H&E staining of papillomas (bar represents 1000 µm) and mice shaved backs (right panel) are shown. B Percentage of papilloma-free mice during the course of the experiment (representative of 4 independent experiments). C Number of tumors in each experimental group classified according to lesion size (total, <2 mm and >2 mm; mean ± SEM; 3 independent experiments) at the end of carcinogenesis protocol. Right panel, results corresponding to papillomas>2 mm are detailed. *p < 0.05. D Ki67 expression in papillomas from Lgals7−/−, WT and Tg46 mice at the end point of carcinogenesis protocol, evaluated by immunohistochemistry. Representative images (left panel; bar represents 100 µm) and quantification of Ki67+ cells (right panel; mean ± SEM; 3 independent experiments) are shown. E Expression of K10, K14 and Gal-7 in papillomas from Tg46, WT and Lgals7−/− mice evaluated by immunohistochemistry. Representative images of 10 samples per group (left panel; bar represents 1 mm) and quantification (right panels; mean ± SEM; 3 independent experiments) are shown. In panel A, p values correspond to the end point of the experiment.