Journal of Skin Cancer / 2013 / Article / Tab 1

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 modelSkin phenotypeSusceptibility to skin carcinogenesisReferences

K5.Cre Stat3flox/−(i) Defective wound healing
(ii) Defective hair cycle from 2nd
anagen onward
Not tested[17]
K5.Cre Stat3flox/floxNo visible phenotypeReduced susceptibility
to both DMBA-TPA and UVB carcinogenesis
[2123]
K5.CreE Stat3flox/floxNo visible phenotypeReduced susceptibility to both tumor initiation with DMBA and tumor promotion with TPA; UVB not tested[24]
K15.CrePR1 Stat3flox/floxNo visible phenotypeReduced susceptibility to tumor initiation by DMBA; UVB not tested[25]
K5.Cre Bcl-xLflox/floxNo visible phenotypeReduced 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]