Document Detail


v-raf suppresses apoptosis and promotes growth of interleukin-3-dependent myeloid cells.
MedLine Citation:
PMID:  8036007     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
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.
Authors:
J L Cleveland; J Troppmair; G Packham; D S Askew; P Lloyd; M González-Garcia; G Nuñez; J N Ihle; U R Rapp
Related Documents :
11920957 - Anoikis is regulated by bcl-2-independent pathways in human prostate carcinoma cells.
17066487 - Truncated midkine correlates with sensitivity to anticancer drugs and malignancy in hum...
11222007 - Bax/bcl-2: cellular modulator of apoptosis in feline skin and basal cell tumours.
12615727 - Bcl-w is expressed in a majority of infiltrative gastric adenocarcinomas and suppresses...
23469687 - Zerumbone induces apoptosis in human renal cell carcinoma via gli-1/bcl-2 pathway.
2875897 - Properties of pc12 pheochromocytoma cells transplanted to the adult rat brain.
Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.    
Journal Detail:
Title:  Oncogene     Volume:  9     ISSN:  0950-9232     ISO Abbreviation:  Oncogene     Publication Date:  1994 Aug 
Date Detail:
Created Date:  1994-08-15     Completed Date:  1994-08-15     Revised Date:  2009-11-19    
Medline Journal Info:
Nlm Unique ID:  8711562     Medline TA:  Oncogene     Country:  ENGLAND    
Other Details:
Languages:  eng     Pagination:  2217-26     Citation Subset:  IM    
Affiliation:
Department of Biochemistry, St. Jude Children's Research Hospital, Memphis, Tennessee 38105.
Export Citation:
APA/MLA Format     Download EndNote     Download BibTex
MeSH Terms
Descriptor/Qualifier:
Animals
Apoptosis*
Bone Marrow Cells*
Cell Division
Cells, Cultured
Genes, myc
Interleukin-3 / physiology*
Mice
Oncogene Proteins v-raf
Proto-Oncogene Proteins / physiology
Proto-Oncogene Proteins c-bcl-2
Retroviridae Proteins, Oncogenic / genetics,  physiology*
Signal Transduction
Grant Support
ID/Acronym/Agency:
DK42932/DK/NIDDK NIH HHS; DK44158/DK/NIDDK NIH HHS; P0 CA21765/CA/NCI NIH HHS
Chemical
Reg. No./Substance:
0/Interleukin-3; 0/Proto-Oncogene Proteins; 0/Proto-Oncogene Proteins c-bcl-2; 0/Retroviridae Proteins, Oncogenic; EC 2.7.11.1/Oncogene Proteins v-raf

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


Previous Document:  Potent SHC tyrosine phosphorylation by epidermal growth factor at low receptor density or in the abs...
Next Document:  The E1A transcriptional control region is efficiently activated in proliferating tissues of transgen...