| First Author | Saez E | Year | 1995 |
| Journal | Cell | Volume | 82 |
| Issue | 5 | Pages | 721-32 |
| PubMed ID | 7545543 | Mgi Jnum | J:78834 |
| Mgi Id | MGI:2386356 | Doi | 10.1016/0092-8674(95)90469-7 |
| Citation | Saez E, et al. (1995) c-fos is required for malignant progression of skin tumors. Cell 82(5):721-32 |
| abstractText | The proto-oncogene c-fos is a major nuclear target for signal transduction pathways involved in the regulation of cell growth, differentiation, and transformation. Using the multistep skin carcinogenesis model, we have directly tested the ability of c-fos-deficient mice to develop cancer. Upon treatment with a tumor promoter, c-fos knockout mice carrying a v-H-ras transgene were able to develop benign tumors with similar kinetics and relative incidence as wild-type animals. However, c-fos-deficient papillomas quickly became very dry and hyperkeratinized, taking on an elongated, horny appearance. While wild-type papillomas eventually progressed into malignant tumors, c-fos-deficient tumors failed to undergo malignant conversion. Experiments in which v-H-ras-expressing keratinocytes were grafted onto nude mice suggest that c-fos-deficient cells have an intrinsic defect that hinders tumorigenesis. These results demonstrate that a member of the AP-1 family of transcription factors is required for the development of a malignant tumor. |
