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. 2019 Nov 21;19(1):e13075. doi: 10.1111/acel.13075

Figure 5.

Figure 5

Cancer resistance in TRPC7 knockout mice. (a) Experimental design for examining the effects of ultraviolet B (UVB) exposure and carcinogens on the epidermis of wild‐type (WT) and TRPC7 knockout mice (TRPC7+/− and TRPC7−/−) for up to 43 weeks. UVB exposure was administered once every 2 days for 43 weeks. At week 29, the carcinogens phorbol myristate acetate (PMA, 7.5 μg) and 7,12‐dimethylbenz(a)anthracene (DMBA, 50 μg) were injected to promote tumor growth. (b) At week 43, dorsal skin and tail skin clippings were sectioned and stained with hematoxylin and eosin. The quantification of the mean (± SD) epidermal thickness in (c) dorsal and (d) tail skin. (e) Tumor formation, including epidermal papilloma and hypodermal sarcoma, was observed in the skin near the carcinogen injection sites. (f) Tumor prevalence and (g) tumor volume (mean ± standard error of the mean) increased with time in all groups of mice but were significantly reduced at 43 weeks in knockout mice compared with wild‐type mice. The expression of (h) KRT10, (i) KRT14, (j) senescence‐associated β‐galactosidase (SA‐β‐gal), and (k) TRPC7 is shown in mouse dorsal skin at the boundary between the epidermis and tumor. *p < .05; **p < .01; ***p < .001