Review Article
Role of Stat3 in Skin Carcinogenesis: Insights Gained from Relevant Mouse Models
Table 1
Mouse models for evaluating Stat3 function in skin carcinogenesis.
| Mouse model | Skin phenotype | Susceptibility to skin carcinogenesis | References |
| K5.Cre Stat3flox/ā | (i) Defective wound healing (ii) Defective hair cycle from 2nd anagen onward | Not tested | [17] | K5.Cre Stat3flox/flox | No visible phenotype | Reduced susceptibility to both DMBA-TPA and UVB carcinogenesis | [21ā23] | K5.CreE Stat3flox/flox | No visible phenotype | Reduced susceptibility to both tumor initiation with DMBA and tumor promotion with TPA; UVB not tested | [24] | K15.CrePR1 Stat3flox/flox | No visible phenotype | Reduced susceptibility to tumor initiation by DMBA; UVB not tested | [25] | K5.Cre Bcl-xLflox/flox | No visible phenotype | Reduced susceptibility to both DMBA-TPA and UVB carcinogenesis | [26] | K5.Stat3C | (i) Enlarged blood vessels in skin at birth (ii) Sparse hair coat (iii) Increased skin vascularization in adult mice (iv) Hypervascularization in response to mild wounding (e.g., tape stripping) (v) Develop scaly, hyperkeratotic lesions on tail (psoriasis) (vi) No spontaneous skin tumors
| Enhanced susceptibility to DMBA-TPA and UVB skin carcinogenesis Enhanced progression of skin tumors to SCCs | [22, 23, 27, 28] |
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