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Beta HPV38 oncoproteins act with a hit-and-run mechanism in ultraviolet radiation-induced skin carcinogenesis in mice

Fig 1

HPV38 E6 and E7 induce an increased steady-state level of UV-induced mutations in mouse skin keratinocytes.

(A) UV-induced cSCCs in K14 HPV38 E6/E7 Tg mice have a vast number of somatic mutations. SCCs display a very high mutational load, with each Tg animal (Tg1–3) harbouring almost 3 times the number of variants compared with pre-malignant lesions (Pre-m). All differences in number of DNA mutations among the tree types of specimens were statistically significant: * ≤0.05; ** ≤0.01; **** ≤0.0001. (B) cSCCs of K14 HPV38 E6/E7 Tg mice display the classic UV-induced mutation signature with a very high number of C:G > T:A mutations. This type of mutation represents the majority of the SNV type in SCC samples of the three Tg animals. (C) Mutation spectrum of pooled SCC samples from the three mice. This spectrum displays the high prevalence of C:G > T:A mutations, especially in the 5′-T_N-3′ and 5′-C_N-3′ context. The y axis represents the percentage of mutations, and the x axis the trinucleotide sequence context.

Fig 1