| First Author | Fleischmann A | Year | 2003 |
| Journal | Cancer Cell | Volume | 4 |
| Issue | 6 | Pages | 477-82 |
| PubMed ID | 14706339 | Mgi Jnum | J:89283 |
| Mgi Id | MGI:3039323 | Doi | 10.1016/s1535-6108(03)00280-0 |
| Citation | Fleischmann A, et al. (2003) Rhabdomyosarcoma development in mice lacking Trp53 and Fos: tumor suppression by the Fos protooncogene. Cancer Cell 4(6):477-82 |
| abstractText | The Fos protein, a major component of the AP-1 transcription factor, is essential for osteoclast differentiation, acts as an oncogene, potentiates transforming signals, and controls invasive growth and angiogenesis during tumor progression. To investigate a potential genetic interaction between the Trp53 and Fos pathways, Trp53/Fos double knockout mice were generated. These mice develop highly proliferative and invasive rhabdomyosarcomas of the facial and orbital regions, with more than 90% penetrance at 6 months of age. Rhabdomyosarcoma cell lines established from the primary tumors express characteristic muscle-specific markers, and reexpression of Fos is associated with enhanced apoptosis in vitro. Moreover, Fos is able to repress Pax7 expression in rhabdomyosarcoma cell lines and primary myoblasts, suggesting a molecular link to genetic alterations involved in human rhabdomyosarcomas. |
