The effects of tumor promoters on HTLV-1 expression in a low-virus producer and a non-virus producer cell line

Carter, Linda J.; Blakeslee, James R.

doi:10.1016/0304-3835(88)90077-8

Cancer Letters

1988

DOI: 10.1016/0304-3835(88)90077-8

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The effects of tumor promoters on HTLV-1 expression in a low-virus producer and a non-virus producer cell line

Linda J. Carter

James R. Blakeslee

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Cited by 3 publications

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“…Other studies have demonstrated that 12-0tetradecanoylphorbol-13-acetate (TPA) can activate the expression of reporter genes directed by the HTLV-I long terminal repeat in transient transfection assays (11,12,18,31,34). However, inconsistent data have been reported regarding the effect of this and other tumor promoters on HTLV expression and replication in infected cells (7,15,16,22,24,40). Therefore, the present study was undertaken to further clarify this issue.…”

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confidence: 91%

Stimulation of virus production and induction of self-syncytium formation in human T-cell leukemia virus type I- and type II-infected T cells by 12-O-tetradecanoylphorbol-13-acetate

Wolfson

Lev

Avinoah

et al. 1994

J Virol

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Treatment of human T-cell leukemia virus type I (HTLV-I)and HTLV-II-infected T-cell lines with 12-0-tetradecanoylphorbol-13-acetate (TPA) stimulated virus release. However, this stimulation was mainly detected at 42 to 48 h of treatment, whereas later virus release declined rapidly. During the first 48 h, TPA had no effect on cell growth, but later, the number of viable cells was profoundly lower in the TPA-treated than in the untreated cultures. This shift in virus release and cell number resulted from self-fusion of a large proportion of the virus-producing cells, which seemed to consequently enter into a dying process. This fusion, which resulted in syncytium formation, was strongly inhibited by anti-HTLV-I env monoclonal antibodies. Furthermore, no self-fusion was detected in three different uninfected T-cell lines similarly treated with TPA. On the other hand, stimulation of virus production by 3-methylcolanthrene (3-MC) treatment failed to induce self-fusion in the infected cells. Moreover, no syncytium was detected when these 3-MC-treated infected cells were cocultured with any of the TPA-treated uninfected cells. The effects of TPA on virus production and syncytium formation were both abolished by three different protein kinase C inhibitors. Taken together, these data suggest that the self-fusion observed in these experiments required both enhanced virus production and protein kinase C-phosphorylated viral or/and virally induced cellular component(s).

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mentioning

confidence: 91%

Stimulation of virus production and induction of self-syncytium formation in human T-cell leukemia virus type I- and type II-infected T cells by 12-O-tetradecanoylphorbol-13-acetate

Wolfson

Lev

Avinoah

et al. 1994

J Virol

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Sp1-p53 Heterocomplex Mediates Activation of HTLV-I Long Terminal Repeat by 12-O-Tetradecanoylphorbol-13-acetate That Is Antagonized by Protein Kinase C

et al. 2001

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We have previously demonstrated that 12-O-tetradecanoylphorbol-13-acetate (TPA) activates human T-cell leukemia virus type-I long terminal repeat (LTR) in Jurkat cells by a protein kinase C (PKC)-independent mechanism involving a posttranslational activation of Sp1 binding to an Sp1 site located within the Ets responsive region-1 (ERR-1). By employing the PKC inhibitor, bisindolylmaleimide I and cotransfecting the reporter LTR construct with a vector expressing PKC-alpha, we demonstrated, in the present study, that this effect of TPA was not only independent of, but actually antagonized by, PKC. Electrophoretic mobility shift assays together with antibody-mediated supershift and immuno-coprecipitation analyses, revealed that the posttranslational activation of Sp1 was exerted by inducing the formation of Sp1-p53 heterocomplex capable of binding to the Sp1 site in ERR-1. Furthermore, we demonstrated that Jurkat cells contain both wild-type (w.t.) and mutant forms of p53 and we detected both of them in this complex at variable combinations; some molecules of the complex contained either the w.t. or the mutant p53 separately, whereas others contained the two of them together. Finally, we showed that the Sp1-p53 complexes could bind also to an Sp1 site present in the promoter of another gene such as the cyclin-dependent kinase inhibitor p21(WAF-1), but not to consensus recognition sequences of the w.t. p53. Therefore, we speculate that there might be several other PKC-independent biological effects of TPA which result from interaction of such Sp1-p53 complexes with Sp1 recognition sites residing in the promoters of a wide variety of cellular and viral genes.

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Interactions between retroviruses and environmental carcinogens and their role in animal and human leukemogenesis

et al. 1992

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The effects of tumor promoters on HTLV-1 expression in a low-virus producer and a non-virus producer cell line

Cited by 3 publications

References 19 publications

Stimulation of virus production and induction of self-syncytium formation in human T-cell leukemia virus type I- and type II-infected T cells by 12-O-tetradecanoylphorbol-13-acetate

Stimulation of virus production and induction of self-syncytium formation in human T-cell leukemia virus type I- and type II-infected T cells by 12-O-tetradecanoylphorbol-13-acetate

Sp1-p53 Heterocomplex Mediates Activation of HTLV-I Long Terminal Repeat by 12-O-Tetradecanoylphorbol-13-acetate That Is Antagonized by Protein Kinase C

Interactions between retroviruses and environmental carcinogens and their role in animal and human leukemogenesis

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