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 × Stat3^flox/−	(i) Defective wound healing; (ii) Defective hair cycle from 2nd; anagen onward	Not tested	[17]
K5.Cre × Stat3^flox/flox	No visible phenotype	Reduced susceptibility; to both DMBA-TPA and UVB carcinogenesis	[21–23]
K5.CreER^T2 × Stat3^flox/flox	No visible phenotype	Reduced susceptibility to both tumor initiation with DMBA and tumor promotion with TPA; UVB not tested	[24]
K15.CrePR1 × Stat3^flox/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]