PMID- 1913629
OWN - NLM
STAT- MEDLINE
DCOM- 19911030
LR  - 20190720
IS  - 0304-3835 (Print)
IS  - 0304-3835 (Linking)
VI  - 60
IP  - 1
DP  - 1991 Oct
TI  - Regulation of cellular trans-activating activities in two different promonocytic 
      leukemia cell lines.
PG  - 75-83
AB  - Trans-activating activities of certain cellular promoter/enhancer genes may 
      reflect the underlying mechanism for cellular differentiation. We have used two 
      promonocytic leukemia cell lines, U937 and HL-CZ, which differ in their 
      differentiation antigen expression. While both cell lines express CD15 antigen, 
      only the former expresses both CD4 and CD10 antigens. These phenotypes suggest 
      that these two cell lines appear to be arrested at different stages of 
      differentiation. Some regions of the long terminal repeat (LTR) of human 
      immunodeficiency virus-1 (HIV-1) contain nucleotide sequences which bind cellular 
      trans-activating factors such as NF-kappa B and Sp1. These sequences are also 
      present in cellular regulatory gene sequences. The cell lines have been 
      transfected by electroporation with a nested series of deletion mutants 
      containing different lengths of the promoter/enhancer region for HIV-LTR. The 
      promoter/enhancer region has been linked to a 'reporter' chloramphenicol acetyl 
      transferase (CAT) gene. We have found that promoter/enhancer trans-activation is 
      markedly enhanced by treating transfected cells with 
      12-O-tetradecanoylphorbol-13-acetate (TPA), while similar treatment with tumor 
      necrosis factor-alpha (TNF alpha) slightly enhanced activation. U937 cells always 
      showed much greater transactivating activities than did HL-CZ cells. Deletion of 
      a negative regulatory element (NRE) from the LTR resulted in an enhanced 
      transactivation, while deletions affecting NF-kappa B and/or Sp1 binding sites 
      markedly reduced transactivation. Deletion of both NRE and NRF, a second negative 
      regulatory factor binding site, from the LTR restored the transactivation. 
      However, in the presence of TPA, deletion of NRE sequence without concomitant 
      deletion of the downstream NRF binding sequence was sufficient for recovering 
      transactivation. Since these two cell lines have shown subtle differences in 
      these responses, it may be speculated that monocytes at different stages of 
      differentiation may respond in different ways, qualitatively and/or 
      quantitatively, to signal transduction factors involved in the transactivation of 
      cellular genes.
FAU - Chang, K S
AU  - Chang KS
AD  - Medical Research Center, Chang Gung Memorial Hospital, Taoyuan, Taiwan, Republic 
      of China.
FAU - Liu, W T
AU  - Liu WT
FAU - Josephs, S F
AU  - Josephs SF
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - Ireland
TA  - Cancer Lett
JT  - Cancer letters
JID - 7600053
RN  - 0 (Antigens, Differentiation)
RN  - 0 (DNA, Neoplasm)
RN  - 0 (Tumor Necrosis Factor-alpha)
RN  - NI40JAQ945 (Tetradecanoylphorbol Acetate)
SB  - IM
MH  - Antigens, Differentiation/analysis
MH  - Base Sequence
MH  - DNA Mutational Analysis
MH  - DNA, Neoplasm/analysis
MH  - *Gene Expression Regulation, Leukemic
MH  - HIV Long Terminal Repeat/genetics
MH  - Humans
MH  - Leukemia, Myeloid/*genetics/immunology
MH  - Molecular Sequence Data
MH  - Plasmids
MH  - Tetradecanoylphorbol Acetate/pharmacology
MH  - Transcriptional Activation/drug effects/*genetics
MH  - Transfection
MH  - Tumor Cells, Cultured/immunology
MH  - Tumor Necrosis Factor-alpha/pharmacology
EDAT- 1991/10/01 00:00
MHDA- 1991/10/01 00:01
CRDT- 1991/10/01 00:00
PHST- 1991/10/01 00:00 [pubmed]
PHST- 1991/10/01 00:01 [medline]
PHST- 1991/10/01 00:00 [entrez]
AID - 0304-3835(91)90051-I [pii]
AID - 10.1016/0304-3835(91)90051-i [doi]
PST - ppublish
SO  - Cancer Lett. 1991 Oct;60(1):75-83. doi: 10.1016/0304-3835(91)90051-i.