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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) increases the expression of Epstein–Barr virus (EBV)-lytic genes and decreases the expression of EBV-latent genes. EBV-positive T cell lines and natural killer (NK) cell lines were treated with 5 μM SAHA (closed triangles) or control (open circles) and cultured for 24 or 48 h. EBV-encoded gene expression was analyzed using real-time RT-PCR. β2-microglobulin was used as a reference gene for relative quantification, and was assigned an arbitrary value of 1 (100). Data are expressed as means ± SEM.
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fig05: Suberoylanilide hydroxamic acid (SAHA) increases the expression of Epstein–Barr virus (EBV)-lytic genes and decreases the expression of EBV-latent genes. EBV-positive T cell lines and natural killer (NK) cell lines were treated with 5 μM SAHA (closed triangles) or control (open circles) and cultured for 24 or 48 h. EBV-encoded gene expression was analyzed using real-time RT-PCR. β2-microglobulin was used as a reference gene for relative quantification, and was assigned an arbitrary value of 1 (100). Data are expressed as means ± SEM.

Mentions: The expression of eight EBV-related genes, including lytic genes (BZLF1 and gp350/220) and latent genes (EBNA1, EBNA2, LMP1, LMP2, EBER1 and Bam HI-A rightward transcripts [BART]) were analyzed using real-time RT-PCR. In the SNT13, KAI3 and SNK6 cell lines, the expression of BZLF1, which is an immediate-early gene in the lytic infection cycle, was increased by SAHA (Fig.5). However, the expression of the late lytic gene gp350/220 was increased only in the SAHA-treated SNT13 cell line. These results indicated that SAHA induced lytic infection in some EBV-positive T and NK cell lines, although it was abortive. The expression of BZLF1 was decreased in the SAHA-treated SNT16 as time went by, while that in mock-treated SNT16 was also decreased. Of the EBV latent genes tested, the expression of EBNA1, LMP1 and BART was decreased in most of the cell lines, whereas that of LMP2 was increased by SAHA (Fig.5). Next, the EBNA1 and LMP1 protein levels were determined by immunoblotting. SAHA decreased the EBNA1 protein level in all cell lines, and that of LMP1 in the SNT16, KAI3 and SNK6 cell lines (Fig.6).


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) increases the expression of Epstein–Barr virus (EBV)-lytic genes and decreases the expression of EBV-latent genes. EBV-positive T cell lines and natural killer (NK) cell lines were treated with 5 μM SAHA (closed triangles) or control (open circles) and cultured for 24 or 48 h. EBV-encoded gene expression was analyzed using real-time RT-PCR. β2-microglobulin was used as a reference gene for relative quantification, and was assigned an arbitrary value of 1 (100). Data are expressed as means ± SEM.
© Copyright Policy - open-access
Related In: Results  -  Collection

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

fig05: Suberoylanilide hydroxamic acid (SAHA) increases the expression of Epstein–Barr virus (EBV)-lytic genes and decreases the expression of EBV-latent genes. EBV-positive T cell lines and natural killer (NK) cell lines were treated with 5 μM SAHA (closed triangles) or control (open circles) and cultured for 24 or 48 h. EBV-encoded gene expression was analyzed using real-time RT-PCR. β2-microglobulin was used as a reference gene for relative quantification, and was assigned an arbitrary value of 1 (100). Data are expressed as means ± SEM.
Mentions: The expression of eight EBV-related genes, including lytic genes (BZLF1 and gp350/220) and latent genes (EBNA1, EBNA2, LMP1, LMP2, EBER1 and Bam HI-A rightward transcripts [BART]) were analyzed using real-time RT-PCR. In the SNT13, KAI3 and SNK6 cell lines, the expression of BZLF1, which is an immediate-early gene in the lytic infection cycle, was increased by SAHA (Fig.5). However, the expression of the late lytic gene gp350/220 was increased only in the SAHA-treated SNT13 cell line. These results indicated that SAHA induced lytic infection in some EBV-positive T and NK cell lines, although it was abortive. The expression of BZLF1 was decreased in the SAHA-treated SNT16 as time went by, while that in mock-treated SNT16 was also decreased. Of the EBV latent genes tested, the expression of EBNA1, LMP1 and BART was decreased in most of the cell lines, whereas that of LMP2 was increased by SAHA (Fig.5). Next, the EBNA1 and LMP1 protein levels were determined by immunoblotting. SAHA decreased the EBNA1 protein level in all cell lines, and that of LMP1 in the SNT16, KAI3 and SNK6 cell lines (Fig.6).

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