PMID- 2496305
OWN - NLM
STAT- MEDLINE
DCOM- 19890607
LR  - 20071115
IS  - 0888-8809 (Print)
IS  - 0888-8809 (Linking)
VI  - 3
IP  - 2
DP  - 1989 Feb
TI  - Induction of macrophage-like differentiation of HL-60 leukemia cells by tumor 
      necrosis factor-alpha: potential role of fos expression.
PG  - 409-19
AB  - Tumor necrosis factor-alpha (TNF-alpha) is a macrophage-derived cytokine elicited 
      during cellular responses to various microbial infections. TNF-alpha exerts 
      direct cytotoxicity toward some tumor cells in vitro and produces hemorrhagic 
      tumor necrosis in vivo. In human promyelocytic HL-60 leukemia cells, human 
      recombinant TNF-alpha (rTNF-alpha) exhibits a small early proliferative effect 
      (within 48 h), followed by marked cytostatic activity at 96 h after the addition 
      of rTNF-alpha. Cytostasis is contiguous with an induction of cell differentiation 
      along the monocyte/macrophage lineage. The cell proliferation effects and the 
      induction of the differentiated phenotype are preceded by an approximate 5-fold 
      increase in c-fos mRNA levels within 90 min after rTNF-alpha treatment of log 
      phase HL-60 cells. Nuclear in vitro transcription assays indicate that the effect 
      of rTNF-alpha on c-fos mRNA abundance is controlled at the transcriptional level. 
      We have also used a postembedding immunocolloidal gold electron microscopy 
      technique to localize and semiquantitate pp55c-fos proto-oncoprotein levels in 
      the nucleus of both control and rTNF-alpha-treated HL-60 leukemia cells. In 
      response to rTNF-alpha, we have observed a rapid and transient accumulation of 
      pp55c-fos in discrete nuclear substructures within 2 h after treatment. C-fos 
      staining appears in clusters, which are preferentially localized over 
      semi-condensed chromatin and interchromatin granules. These results suggest that 
      pp55c-fos is involved in the signal transduction system initiated by rTNF-alpha 
      during the induction of HL-60 differentiation.
FAU - Squinto, S P
AU  - Squinto SP
AD  - Department of Biochemistry and Molecular Biology, Louisiana State University 
      Medical Center, New Orleans 70119.
FAU - Doucet, J P
AU  - Doucet JP
FAU - Block, A L
AU  - Block AL
FAU - Morrow, S L
AU  - Morrow SL
FAU - Davenport, W D Jr
AU  - Davenport WD Jr
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - United States
TA  - Mol Endocrinol
JT  - Molecular endocrinology (Baltimore, Md.)
JID - 8801431
RN  - 0 (Proto-Oncogene Proteins)
RN  - 0 (Proto-Oncogene Proteins c-fos)
RN  - 0 (RNA, Messenger)
RN  - 0 (Tumor Necrosis Factor-alpha)
SB  - IM
MH  - Cell Line
MH  - Cell Nucleus/analysis/pathology/ultrastructure
MH  - Cell Transformation, Neoplastic/*drug effects
MH  - *Gene Expression Regulation
MH  - Humans
MH  - Leukemia, Myeloid, Acute/*pathology
MH  - Macrophages/*pathology/ultrastructure
MH  - Microscopy, Electron/methods
MH  - Proto-Oncogene Proteins/analysis/*genetics
MH  - Proto-Oncogene Proteins c-fos
MH  - RNA, Messenger/analysis
MH  - Transcription, Genetic/drug effects
MH  - Tumor Cells, Cultured/drug effects
MH  - Tumor Necrosis Factor-alpha/analysis/*pharmacology
EDAT- 1989/02/01 00:00
MHDA- 2001/03/28 10:01
CRDT- 1989/02/01 00:00
PHST- 1989/02/01 00:00 [pubmed]
PHST- 2001/03/28 10:01 [medline]
PHST- 1989/02/01 00:00 [entrez]
AID - 10.1210/mend-3-2-409 [doi]
PST - ppublish
SO  - Mol Endocrinol. 1989 Feb;3(2):409-19. doi: 10.1210/mend-3-2-409.