Figure 3. IL‐38 promotes inflammation‐driven tumorigenesis in vivo and in vitro .
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ARepresentative immunohistochemical staining micrographs of γH2AX in the skin of Il‐38f / f (n = 5) and K14Cre /+ ‐Il‐38f / f (n = 5) mice after treated with DMBA for 24 h. Red triangles indicate the γH2AX+ positive cells. Scale bars represent 100 μm. The graph shows the number of γH2AX+ cells per high‐powered field.
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BTaqman qPCR analysis of Hras codon‐61 mutations in DMBA‐treated skin of Il‐38f / f (n = 5) and K14Cre /+ ‐Il‐38f / f (n = 5) mice after treated with DMBA for 24 h.
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C, DThe dorsal hair of normal C57/BL6 mice was shaved and treated with DMBA/TPA twice a week for 3 weeks to induce the skin inflammation. (C) Percentage of skin‐infiltrating immune cell subsets within total live cells were determined using flow cytometry in DMBA/TPA‐treated Il‐38f / f (n = 5) and K14Cre /+ ‐Il‐38f / f mice (n = 5). (D) Relative expression levels of inflammatory mediators in the skin of DMBA/TPA‐treated Il‐38f / f (n = 5) and K14Cre /+ ‐Il‐38f / f mice (n = 5) were quantified using qPCR.
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E, FRelative expression of inflammatory cytokines in A431 cells after Il‐38 overexpression (E) or knockdown (F) was detected using qPCR.
Data information: Error bars represent the mean ± SD. All data are biological replicates. *P < 0.05; **P < 0.01; ***P < 0.001; P values were calculated using Student’s t‐test.