Stimulation of HTLV-I expression by subtoxic dose of 3-methylcholanthrene

Feldman, Gleb; Aboud, Mordechai

doi:10.1016/0145-2126(93)90098-6

Leukemia Research

1993

DOI: 10.1016/0145-2126(93)90098-6

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Stimulation of HTLV-I expression by subtoxic dose of 3-methylcholanthrene

Gleb Feldman

Mordechai Aboud

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Cited by 2 publications

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“…In addition, we compared the effects of TPA and 3-MC on the level of the viral env proteins within SLB-I cells. These proteins were quantitated in cell extracts by Western blot (immunoblot) analysis, using the above-mentioned anti-HTLV-I env monoclonal antibody in conjunction with horseradish peroxidase-conjugated goat anti-mouse immunoglobulin G antibodies as described elsewhere (10). Figure 3 shows that the level of these proteins was considerably increased after treatment with either of these agents, and the extent of this increase was comparable for both agents.…”

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confidence: 99%

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: 99%

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 Is Involved in a Protein Kinase C-Independent Activation of Human T Cell Leukemia Virus Type I Long Terminal Repeat by 12-O-Tetradecanoylphorbol-13-acetate

1999

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The long terminal repeat (LTR) of human T cell leukemia virus type-I (HTLV-I) contains binding sites for several cellular transcription factors that can activate its expression independently of the viral transactivator Tax protein. In a previous study, we have shown that 12-O-tetradecanoylphorbol-13-acetate (TPA) induces a Tax-independent activation of the viral LTR expression. We have also noted that although most other TPA biological effects are attributed to its protein kinase C (PKC)-activating potential, this particular effect of TPA is PKC independent and antagonized by PKC activity. In addition, we have demonstrated that deletion of the ets-responsive region 1 (ERR-1) from the LTR abolishes its response to TPA. In the present study, we demonstrate that TPA exerts this effect by enhancing the binding of the Sp1 transcription factor to an Sp1-binding site located within ERR-1. This Sp1-binding stimulation was not diminished by a potent PKC-specific inhibitor like bisindolylmaleimide-I, indicating that it did not depend on PKC activity. However, no increase in Sp1 protein level could be detected in the TPA-treated cells, suggesting that TPA exerted its effect by a posttranslational modification of Sp1 protein rather than by stimulating its synthesis. Although the proximal Tax responsive 21-bp element also contains an Sp1-binding site, the present study shows that the modified Sp1 protein mediates the TPA effect on LTR only through the Sp1 site of the ERR-1.

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Stimulation of HTLV-I expression by subtoxic dose of 3-methylcholanthrene

Cited by 2 publications

References 21 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 Is Involved in a Protein Kinase C-Independent Activation of Human T Cell Leukemia Virus Type I Long Terminal Repeat by 12-O-Tetradecanoylphorbol-13-acetate

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