The effects of vinblastine on the expression of human immunodeficiency virus type 1 long terminal repeat

Ender Akan; Chin Mei Chang-Liu; Jobu Watanabe; Kota Ishizawa; Gayle E. Woloschak

doi:10.1016/S0145-2126(96)00125-7

The effects of vinblastine on the expression of human immunodeficiency virus type 1 long terminal repeat

Ender Akan, Chin Mei Chang-Liu, Jobu Watanabe, Kota Ishizawa, Gayle E. Woloschak^*

^*Corresponding author for this work

Radiation Oncology

Research output: Contribution to journal › Article › peer-review

4 Scopus citations

Abstract

Previous work by our group has demonstrated induction of the HIV-LTR following exposure of cells to various DNA-damaging agents such as ultraviolet (UV) light, cisplatin, and doxorubicin. The current experiments were designed to determine the relative effects of the anti-mitotic drug vinblastine on expression of the HIV-LTR. Using human cervical carcinoma (HeLa) cells stably transfected with the chloramphenicol acetyl transferase (CAT) reporter transcriptionally driven by the HIV-LTR promoter, we demonstrated a 9-10-fold induction at 48-72 h following vinblastine treatment. Previous experiments had demonstrated repression of cisplatin or doxorubicin-mediated HIV induction by treatment with salicylic acid. The vinblastine induction also was repressed by salicylic acid treatment, but not by treatment with indomethacin, suggesting a role for the NFκB pathway in the inductive response. When UV exposure was coupled to the vinblastine treatment, there was no additive or synergistic effect evident, suggesting similar paths of induction between the two agents. Northern blots demonstrated that these agents were operating at the level of transcription and that salicylic acid inhibited vinblastine-mediated induction of HIV-LTR-CAT mRNA only if administered at the same time as vinblastine; addition of salicylic acid 2 h later had no effect on transcript accumulation. All combinations of treatments with vinblastine and/or salicylic acid markedly reduced cell survival.

Original language	English (US)
Pages (from-to)	459-464
Number of pages	6
Journal	Leukemia Research
Volume	21
Issue number	5
DOIs	https://doi.org/10.1016/S0145-2126(96)00125-7
State	Published - May 1997

Funding

Acknowledgements-The authors thank MS Felicia King for excellent secretarial assistance and Drs David Grdina and Frank Collart for review of this manuscript prior to publication. This work was supported by the U.S. Department of Energy, Office of Health and Environmental Research, under Contract No. W-31-109-ENG-38.

Keywords

DNA-damaging agents
Gene expression
HIV expression
Salicylic acid
Vinblastine

ASJC Scopus subject areas

Hematology
Oncology
Cancer Research

UN SDGs

This output contributes to the following UN Sustainable Development Goals (SDGs)

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10.1016/S0145-2126(96)00125-7

Cite this

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title = "The effects of vinblastine on the expression of human immunodeficiency virus type 1 long terminal repeat",

abstract = "Previous work by our group has demonstrated induction of the HIV-LTR following exposure of cells to various DNA-damaging agents such as ultraviolet (UV) light, cisplatin, and doxorubicin. The current experiments were designed to determine the relative effects of the anti-mitotic drug vinblastine on expression of the HIV-LTR. Using human cervical carcinoma (HeLa) cells stably transfected with the chloramphenicol acetyl transferase (CAT) reporter transcriptionally driven by the HIV-LTR promoter, we demonstrated a 9-10-fold induction at 48-72 h following vinblastine treatment. Previous experiments had demonstrated repression of cisplatin or doxorubicin-mediated HIV induction by treatment with salicylic acid. The vinblastine induction also was repressed by salicylic acid treatment, but not by treatment with indomethacin, suggesting a role for the NFκB pathway in the inductive response. When UV exposure was coupled to the vinblastine treatment, there was no additive or synergistic effect evident, suggesting similar paths of induction between the two agents. Northern blots demonstrated that these agents were operating at the level of transcription and that salicylic acid inhibited vinblastine-mediated induction of HIV-LTR-CAT mRNA only if administered at the same time as vinblastine; addition of salicylic acid 2 h later had no effect on transcript accumulation. All combinations of treatments with vinblastine and/or salicylic acid markedly reduced cell survival.",

keywords = "DNA-damaging agents, Gene expression, HIV expression, Salicylic acid, Vinblastine",

author = "Ender Akan and Chang-Liu, {Chin Mei} and Jobu Watanabe and Kota Ishizawa and Woloschak, {Gayle E.}",

note = "Funding Information: Acknowledgements-The authors thank MS Felicia King for excellent secretarial assistance and Drs David Grdina and Frank Collart for review of this manuscript prior to publication. This work was supported by the U.S. Department of Energy, Office of Health and Environmental Research, under Contract No. W-31-109-ENG-38.",

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AU - Woloschak, Gayle E.

N1 - Funding Information: Acknowledgements-The authors thank MS Felicia King for excellent secretarial assistance and Drs David Grdina and Frank Collart for review of this manuscript prior to publication. This work was supported by the U.S. Department of Energy, Office of Health and Environmental Research, under Contract No. W-31-109-ENG-38.

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N2 - Previous work by our group has demonstrated induction of the HIV-LTR following exposure of cells to various DNA-damaging agents such as ultraviolet (UV) light, cisplatin, and doxorubicin. The current experiments were designed to determine the relative effects of the anti-mitotic drug vinblastine on expression of the HIV-LTR. Using human cervical carcinoma (HeLa) cells stably transfected with the chloramphenicol acetyl transferase (CAT) reporter transcriptionally driven by the HIV-LTR promoter, we demonstrated a 9-10-fold induction at 48-72 h following vinblastine treatment. Previous experiments had demonstrated repression of cisplatin or doxorubicin-mediated HIV induction by treatment with salicylic acid. The vinblastine induction also was repressed by salicylic acid treatment, but not by treatment with indomethacin, suggesting a role for the NFκB pathway in the inductive response. When UV exposure was coupled to the vinblastine treatment, there was no additive or synergistic effect evident, suggesting similar paths of induction between the two agents. Northern blots demonstrated that these agents were operating at the level of transcription and that salicylic acid inhibited vinblastine-mediated induction of HIV-LTR-CAT mRNA only if administered at the same time as vinblastine; addition of salicylic acid 2 h later had no effect on transcript accumulation. All combinations of treatments with vinblastine and/or salicylic acid markedly reduced cell survival.

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The effects of vinblastine on the expression of human immunodeficiency virus type 1 long terminal repeat

Abstract

Funding

Keywords

ASJC Scopus subject areas

UN SDGs

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