Table 1.
Mouse models for evaluating Stat3 function in skin carcinogenesis.
| Mouse model | Skin phenotype | Susceptibility to skin carcinogenesis | References |
|---|---|---|---|
| K5.Cre × Stat3flox/− | (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 |
[21–23] |
| K5.CreERT2× 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-xL flox/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] |