| First Author | Cleveland JL | Year | 1994 |
| Journal | Oncogene | Volume | 9 |
| Issue | 8 | Pages | 2217-26 |
| PubMed ID | 8036007 | Mgi Jnum | J:19420 |
| Mgi Id | MGI:67590 | Citation | Cleveland JL, et al. (1994) v-raf suppresses apoptosis and promotes growth of interleukin-3-dependent myeloid cells. Oncogene 9(8):2217-26 |
| abstractText | Interleukin-3 (IL-3) is required for the proliferation, survival and differentiation of myeloid progenitors. In the absence of IL-3, murine myeloid 32D.3 cells accumulate in the G1 phase of the cell cycle and subsequently undergo programmed cell death, or apoptosis. Here we demonstrate that enforced expression of the v-raf oncogene suppresses apoptosis of myeloid 32D.3 cells following the withdrawal of IL-3. Surprisingly, steady state levels of Bcl-2, an oncogene known to suppress apoptosis, were not dependent upon IL-3 in 32D.3 cells and its levels were not augmented in v-raf clones. This suggests that ability of v-raf to suppress apoptosis in the absence of ligand is either Bcl-2 independent or that v-raf kinase promotes Bcl-2 function. v-raf also promoted growth of these cells in the presence of IL-3. v-raf clones proliferated at an increased rate due to a shortened G1 phase and had decreased requirements for IL-3 for growth. Therefore, transformation of myeloid cells by v-raf involves signaling pathways which promote both cell cycle progression and cell survival. |
