| First Author | Oskarsson T | Year | 2006 |
| Journal | Genes Dev | Volume | 20 |
| Issue | 15 | Pages | 2024-9 |
| PubMed ID | 16882980 | Mgi Jnum | J:111139 |
| Mgi Id | MGI:3653079 | Doi | 10.1101/gad.381206 |
| Citation | Oskarsson T, et al. (2006) Skin epidermis lacking the c-myc gene is resistant to Ras-driven tumorigenesis but can reacquire sensitivity upon additional loss of the p21Cip1 gene. Genes Dev 20(15):2024-9 |
| abstractText | The target gene(s) required for Myc-mediated tumorigenesis are still elusive. Here we show that while endogenous c-Myc is surprisingly dispensable for skin homeostasis and TPA-induced hyperplasia, c-Myc-deficient epidermis is resistant to Ras-mediated DMBA/TPAinduced tumorigenesis. This is mechanistically linked to p21(Cip1), which is induced in tumors by the activated Ras-ERK pathway but repressed by c-Myc. Acute elimination of c-Myc in established tumors leads to the up-regulation of p21(Cip1), and epidermis lacking both p21(Cip1) and c-Myc reacquires normal sensitivity to DMBA/TPA-induced tumorigenesis. This identifies c-Myc-mediated repression of p21(Cip1) as a key step for Ras-driven epidermal tumorigenesis. |
