| First Author | Cho SH | Year | 2001 |
| Journal | Int J Mol Med | Volume | 7 |
| Issue | 3 | Pages | 235-41 |
| PubMed ID | 11179500 | Mgi Jnum | J:67487 |
| Mgi Id | MGI:1930730 | Doi | 10.3892/ijmm.7.3.235 |
| Citation | Cho SH, et al. (2001) Bax gene disruption alters the epidermal response to ultraviolet irradiation and in vivo induced skin carcinogenesis. Int J Mol Med 7(3):235-41 |
| abstractText | Bcl-2 family member proteins are differentially expressed in skin and in non-melanoma skin cancer (NMSC). To elucidate the contribution of bcl-2 and bax proteins to epidermal differentiation and skin carcinogenesis, we investigated keratinocyte proliferation, differentiation and tumourigenesis in bcl-2-/- and bax-/- mice. The rate and pattern of proliferation and spontaneous cell death in the bcl-2-/- and bax-/- mice were not different from control mice. The epidermis of bcl-2-/- and bax-/- expressed sightly higher levels of cytokeratin 1 and loricrin compared to control littermates. The apoptotic response to ultraviolet-induced genotoxic stress was assessed by quantitating TUNEL positive cells. Bax-/- keratinocytes showed a significant resistance to UV-induced cell death compared to control mice. The life-span of bcl-2-/- mice precluded an assessment of bcl-2 gene disruption on in vivo tumourigenesis. A significant increase in tumour incidence was observed in bax-/- mice compared to control mice in two-step chemical carcinogenesis studies. These findings suggest that bcl-2 and bax gene products may be important determinants of normal keratinocyte differentiation and response to genotoxic stress in vivo, and indicate that bax may provide a tumour suppressor effect during skin carcinogenesis. |
