PMID- 10845928
OWN - NLM
STAT- MEDLINE
DCOM- 20000810
LR  - 20210216
IS  - 0006-4971 (Print)
IS  - 0006-4971 (Linking)
VI  - 95
IP  - 12
DP  - 2000 Jun 15
TI  - Constitutive activation of transcription factor AP-1 in primary adult T-cell 
      leukemia cells.
PG  - 3915-21
AB  - Human T-cell leukemia virus type-I (HTLV-I) is the etiologic agent of adult 
      T-cell leukemia (ATL). This study examined the status of the oncogenic 
      transcription factor AP-1 in leukemic cells freshly isolated from patients with 
      ATL. Leukemic cells from peripheral blood of all patients with ATL exhibited 
      constitutive AP-1 DNA binding activity, whereas mononuclear cells from normal 
      individuals did not. In agreement with previous studies, HTLV-I transforming 
      protein, Tax, was found to stimulate the DNA binding activity of AP-1 in a T-cell 
      line. However, HTLV-I genes, including Tax, were not significantly expressed in 
      leukemic cells freshly obtained from patients with ATL. Moreover, all T-cell 
      lines derived from leukemic cells of patients with ATL also displayed 
      constitutive AP-1 DNA binding activity, but expressed little Tax protein. Thus, 
      leukemic cells of patients with ATL appear to have Tax-independent mechanisms 
      that induce AP-1 activity, both in vivo and in vitro. In antibody supershift 
      experiments, AP-1 in fresh leukemic cells and ATL-derived cell lines were found 
      to contain JunD. Consistently, all primary ATL cells and ATL-derived cell lines 
      expressed high levels of JunD messenger RNA. Our results suggest that AP-1 is 
      activated in leukemic cells of patients with ATL through a Tax-independent 
      mechanism and this may play a role in the deregulated phenotypes of ATL leukemic 
      cells. (Blood. 2000;95:3915-3921)
FAU - Mori, N
AU  - Mori N
AD  - Department of Preventive Medicine and AIDS Research, Institute of Tropical 
      Medicine, Nagasaki University, Nagasaki, Japan. n-mori@net.nagasaki-u.ac.jp
FAU - Fujii, M
AU  - Fujii M
FAU - Iwai, K
AU  - Iwai K
FAU - Ikeda, S
AU  - Ikeda S
FAU - Yamasaki, Y
AU  - Yamasaki Y
FAU - Hata, T
AU  - Hata T
FAU - Yamada, Y
AU  - Yamada Y
FAU - Tanaka, Y
AU  - Tanaka Y
FAU - Tomonaga, M
AU  - Tomonaga M
FAU - Yamamoto, N
AU  - Yamamoto N
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - United States
TA  - Blood
JT  - Blood
JID - 7603509
RN  - 0 (Gene Products, tax)
RN  - 0 (Proto-Oncogene Proteins c-jun)
RN  - 0 (Transcription Factor AP-1)
SB  - IM
MH  - Adult
MH  - Cell Line
MH  - Cell Nucleus/metabolism
MH  - Gene Expression Regulation
MH  - Gene Products, tax/metabolism
MH  - Genes, jun
MH  - Genes, pX
MH  - Human T-lymphotropic virus 1/genetics/*physiology
MH  - Humans
MH  - Jurkat Cells
MH  - Leukemia-Lymphoma, Adult T-Cell/*genetics/metabolism
MH  - Proto-Oncogene Proteins c-jun/metabolism
MH  - T-Lymphocytes/metabolism/virology
MH  - Transcription Factor AP-1/*metabolism
MH  - Transcriptional Activation
MH  - Transfection
MH  - Tumor Cells, Cultured
EDAT- 2000/06/14 09:00
MHDA- 2000/08/12 11:00
CRDT- 2000/06/14 09:00
PHST- 2000/06/14 09:00 [pubmed]
PHST- 2000/08/12 11:00 [medline]
PHST- 2000/06/14 09:00 [entrez]
AID - S0006-4971(20)63965-9 [pii]
PST - ppublish
SO  - Blood. 2000 Jun 15;95(12):3915-21.