UV induces CIRP expression and subsequent Stat3 activation, but the biological function and mechanism of CIRP and Stat3 in mediating UVB-induced skin carcinogenesis have not been fully elucidated.
The identification of transcription factors, mainly nuclear factor-kappa B (NF-κB), signal transducer and activator of transcription 3 (STAT3), hypoxia-inducible factor-1 alpha (HIF-1α) and their gene products i.e. prostaglandins, cyclooxygenase-2 (COX-2), cytokines [tumor necrosis factor- alpha (TNF-α)], chemokines [CXC-chemokine ligand (CXCL)] and chemokine receptors suggest critical role of inflammation in skin carcinogenesis.
In this study, we investigate the in vivo role of Stat3 in HPV8-induced skin carcinogenesis by combining our established experimental model of HPV8-induced skin cancer with epidermis-restricted Stat3 ablation.