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. 2021 Aug 31;13(17):4395. doi: 10.3390/cancers13174395

Figure 4.

Figure 4

Co-expression of LEKTI with matriptase in basal keratinocytes delays the onset and progression of chemically induced carcinogenesis. (A) One-stage chemical carcinogenesis scheme: dorsal skin of mice was exposed 5 times to 25 μg of DMBA, starting at week 5 of age, every 3 weeks, and were followed for up to 48 weeks of age. WT (n = 20), K5-LEKTI+/0 (n = 17), K5-Matriptase+/0 (n = 11), and K5-Matriptase+/0/K5-LEKTI+/0 (n = 16). (B) Kaplan–Meier analysis of tumor-free survival. WT (black upside-down triangle), K5-LEKTI+/0 (orange squares), K5-Matriptase+/0 (purple dots), and K5-Matriptase+/0/K5-LEKTI+/0 (green triangles). (C,D) Matriptase induced tumor progression in K5-Matriptase+/0, and K5-Matriptase+/0/K5-LEKTI+/0 mice. Data are expressed in mean ± SD. (C) number of lesions and (D) percentage of lesion of each size in littermate K5-Matriptase+/0 (purple dots) and K5-Matriptase+/0/K5-LEKTI+/0 (green triangles) mice from 14 to 26 weeks of age. p-values (multiple t-tests) are displayed in the graphs. (E) Representative images of the outward appearance of littermate WT, K5-LEKTI+/0, K5-Matriptase+/0, and K5-Matriptase+/0/K5-LEKTI+/0 mice at 26 weeks of age. (F) Klk5 IHC staining of the skin of 3-month-old WT, K5-LEKTI+/0, K5-Matriptase+/0, and K5-Matriptase+/0/LEKTI+/0 mice. Black arrowheads indicate stained areas; Negative secondary antibody control; Bar = 100 μm.