PMID- 10318796
OWN - NLM
STAT- MEDLINE
DCOM- 19990617
LR  - 20210209
IS  - 0021-9258 (Print)
IS  - 0021-9258 (Linking)
VI  - 274
IP  - 20
DP  - 1999 May 14
TI  - Tumor necrosis factor-alpha-induced proliferation of human Mo7e leukemic cells 
      occurs via activation of nuclear factor kappaB transcription factor.
PG  - 13877-85
AB  - Tumor necrosis factor-alpha (TNF-alpha) stimulates proliferation of Mo7e, CMK, 
      HU-3, and M-MOK human leukemic cell lines. We report here the signal transduction 
      pathway involved in TNF-alpha-induced Mo7e cell proliferation. Mo7e cells 
      spontaneously die in the absence of growth factors, but treating the cells with 
      interleukin (IL)-3, IL-6, thrombopoietin, granulocyte/macrophage 
      colony-stimulating factor, or TNF-alpha promotes their survival and 
      proliferation. Although most of these factors activate MAP kinase and Jun 
      NH2-terminal kinase/signal transducer and activators of transcription signaling 
      pathways, TNF-alpha fails to activate either pathway. When Mo7e cells were 
      treated with TNF-alpha, nuclear factor kappaB (NF-kappaB) was activated 
      transiently. The activated NF-kappaB consisted of heterodimers of p65 and p50 
      subunits. The degradation of IkappaBalpha coincided with activation of NF-kappaB 
      in TNF-alpha-treated cells. To investigate the role of activated NF-kappaB in 
      TNF-alpha-induced Mo7e proliferation, a cell-permeable peptide (SN50) carrying 
      the nuclear localization sequence of p50 NF-kappaB was used to block nuclear 
      translocation of activated NF-kappaB. Pretreating Mo7e cells with SN50 blocked 
      TNF-alpha-induced nuclear translocation of NF-kappaB and inhibited 
      TNF-alpha-induced Mo7e cell survival and proliferation. A mutant SN50 peptide did 
      not affect TNF-alpha-induced Mo7e cell growth. SN50 had no effects on IL-3- or 
      granulocyte/macrophage colony-stimulating factor-induced Mo7e cell proliferation. 
      The results indicate that activation of NF-kappaB is involved in 
      TNF-alpha-induced Mo7e cell survival and proliferation.
FAU - Liu, R Y
AU  - Liu RY
AD  - Division of Medical Oncology and Hematology, and Departments of 
      Biochemistry/Molecular Biology and Anatomy, University of South Florida and the 
      H. Lee Moffitt Cancer Center and Research Institute, Tampa, Florida 33612, USA. 
      liur@moffitt.usf.edu
FAU - Fan, C
AU  - Fan C
FAU - Olashaw, N E
AU  - Olashaw NE
FAU - Wang, X
AU  - Wang X
FAU - Zuckerman, K S
AU  - Zuckerman KS
LA  - eng
GR  - CA56072/CA/NCI NIH HHS/United States
GR  - P30 CA76292/CA/NCI NIH HHS/United States
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PT  - Research Support, U.S. Gov't, P.H.S.
PL  - United States
TA  - J Biol Chem
JT  - The Journal of biological chemistry
JID - 2985121R
RN  - 0 (DNA-Binding Proteins)
RN  - 0 (Interleukin-3)
RN  - 0 (Milk Proteins)
RN  - 0 (NF-kappa B)
RN  - 0 (Peptides)
RN  - 0 (SN50 peptide)
RN  - 0 (STAT5 Transcription Factor)
RN  - 0 (Trans-Activators)
RN  - 0 (Tumor Necrosis Factor-alpha)
RN  - 83869-56-1 (Granulocyte-Macrophage Colony-Stimulating Factor)
RN  - EC 2.7.11.17 (Calcium-Calmodulin-Dependent Protein Kinases)
RN  - EC 2.7.11.24 (JNK Mitogen-Activated Protein Kinases)
RN  - EC 2.7.11.24 (Mitogen-Activated Protein Kinases)
SB  - IM
MH  - Calcium-Calmodulin-Dependent Protein Kinases/metabolism
MH  - Cell Division
MH  - Cell Nucleus/metabolism
MH  - DNA-Binding Proteins/metabolism
MH  - Granulocyte-Macrophage Colony-Stimulating Factor/metabolism
MH  - Humans
MH  - Interleukin-3/metabolism
MH  - JNK Mitogen-Activated Protein Kinases
MH  - *Milk Proteins
MH  - *Mitogen-Activated Protein Kinases
MH  - NF-kappa B/antagonists & inhibitors/*metabolism
MH  - Peptides/metabolism
MH  - STAT5 Transcription Factor
MH  - Trans-Activators/metabolism
MH  - Tumor Cells, Cultured
MH  - Tumor Necrosis Factor-alpha/*pharmacology
EDAT- 1999/05/13 00:00
MHDA- 1999/05/13 00:01
CRDT- 1999/05/13 00:00
PHST- 1999/05/13 00:00 [pubmed]
PHST- 1999/05/13 00:01 [medline]
PHST- 1999/05/13 00:00 [entrez]
AID - S0021-9258(19)73248-7 [pii]
AID - 10.1074/jbc.274.20.13877 [doi]
PST - ppublish
SO  - J Biol Chem. 1999 May 14;274(20):13877-85. doi: 10.1074/jbc.274.20.13877.