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Anti-tumor effects of suberoylanilide hydroxamic acid on Epstein-Barr virus-associated T cell and natural killer cell lymphoma.

Siddiquey MN, Nakagawa H, Iwata S, Kanazawa T, Suzuki M, Imadome K, Fujiwara S, Goshima F, Murata T, Kimura H - Cancer Sci. (2014)

Bottom Line: Recent studies have reported that histone deacetylase (HDAC) inhibitors exert anticancer effects against various tumor cells.In addition, SAHA increased the expression of EBV-lytic genes and decreased the expression of EBV-latent genes.SAHA displayed a marked suppressive effect against EBV-associated T and NK cell lymphomas through either induction of apoptosis or cell cycle arrest, and may represent an alternative treatment option.

View Article: PubMed Central - PubMed

Affiliation: Department of Virology, Nagoya University Graduate School of Medicine, Nagoya, Japan.

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Related in: MedlinePlus

Suberoylanilide hydroxamic acid (SAHA) arrests the cell cycle in T and natural killer (NK) cell lines. After treatment with the indicated concentrations of SAHA for 48 h, T and NK cell lines were fixed and stained with propidium iodide. Cell cycle profiles were assessed by flow cytometry. *Because of cell death, the cell cycle assay was indeterminable.
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fig04: Suberoylanilide hydroxamic acid (SAHA) arrests the cell cycle in T and natural killer (NK) cell lines. After treatment with the indicated concentrations of SAHA for 48 h, T and NK cell lines were fixed and stained with propidium iodide. Cell cycle profiles were assessed by flow cytometry. *Because of cell death, the cell cycle assay was indeterminable.

Mentions: To determine whether apoptosis was induced by SAHA in the tested cell lines, early apoptotic cells were quantified by annexin V and 7-AAD staining. SAHA increased early apoptotic cells in the Jurkat, KAI3 and KHYG1 cell lines (Fig.3a). In other cell lines, the proportions of early apoptotic cells were not increased. Next, the cleavage of PARP was analyzed by immunoblotting. With the exception of the SNT16 cell line, SAHA induced the cleavage of PARP in the five cell lines (Fig.3b). Next, effects on the cell cycle were investigated. In the SNT16 and KAI3 cell lines, the population of cells in G1 phase was increased, whereas that in G2 phase was increased in the SNK6 cell line (Fig.4). In Jurkat and KHYG1 cells, the cell cycle assay was indeterminate because of the massive cell death caused by SAHA.


Anti-tumor effects of suberoylanilide hydroxamic acid on Epstein-Barr virus-associated T cell and natural killer cell lymphoma.

Siddiquey MN, Nakagawa H, Iwata S, Kanazawa T, Suzuki M, Imadome K, Fujiwara S, Goshima F, Murata T, Kimura H - Cancer Sci. (2014)

Suberoylanilide hydroxamic acid (SAHA) arrests the cell cycle in T and natural killer (NK) cell lines. After treatment with the indicated concentrations of SAHA for 48 h, T and NK cell lines were fixed and stained with propidium iodide. Cell cycle profiles were assessed by flow cytometry. *Because of cell death, the cell cycle assay was indeterminable.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4317897&req=5

fig04: Suberoylanilide hydroxamic acid (SAHA) arrests the cell cycle in T and natural killer (NK) cell lines. After treatment with the indicated concentrations of SAHA for 48 h, T and NK cell lines were fixed and stained with propidium iodide. Cell cycle profiles were assessed by flow cytometry. *Because of cell death, the cell cycle assay was indeterminable.
Mentions: To determine whether apoptosis was induced by SAHA in the tested cell lines, early apoptotic cells were quantified by annexin V and 7-AAD staining. SAHA increased early apoptotic cells in the Jurkat, KAI3 and KHYG1 cell lines (Fig.3a). In other cell lines, the proportions of early apoptotic cells were not increased. Next, the cleavage of PARP was analyzed by immunoblotting. With the exception of the SNT16 cell line, SAHA induced the cleavage of PARP in the five cell lines (Fig.3b). Next, effects on the cell cycle were investigated. In the SNT16 and KAI3 cell lines, the population of cells in G1 phase was increased, whereas that in G2 phase was increased in the SNK6 cell line (Fig.4). In Jurkat and KHYG1 cells, the cell cycle assay was indeterminate because of the massive cell death caused by SAHA.

Bottom Line: Recent studies have reported that histone deacetylase (HDAC) inhibitors exert anticancer effects against various tumor cells.In addition, SAHA increased the expression of EBV-lytic genes and decreased the expression of EBV-latent genes.SAHA displayed a marked suppressive effect against EBV-associated T and NK cell lymphomas through either induction of apoptosis or cell cycle arrest, and may represent an alternative treatment option.

View Article: PubMed Central - PubMed

Affiliation: Department of Virology, Nagoya University Graduate School of Medicine, Nagoya, Japan.

Show MeSH
Related in: MedlinePlus