Anti‐tumor effects of suberoylanilide hydroxamic acid on Epstein–Barr virus‐associated T cell and natural killer cell lymphoma
The ubiquitous Epstein–Barr virus (EBV) infects not only B cells but also T cells and natural killer (NK) cells and is associated with various lymphoid malignancies. Recent studies have reported that histone deacetylase (HDAC) inhibitors exert anticancer effects against various tumor cells. In the p...
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Published in | Cancer science Vol. 105; no. 6; pp. 713 - 722 |
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Main Authors | , , , , , , , , , |
Format | Journal Article |
Language | English |
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England
John Wiley & Sons, Inc
01.06.2014
BlackWell Publishing Ltd |
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Abstract | The ubiquitous Epstein–Barr virus (EBV) infects not only B cells but also T cells and natural killer (NK) cells and is associated with various lymphoid malignancies. Recent studies have reported that histone deacetylase (HDAC) inhibitors exert anticancer effects against various tumor cells. In the present study, we have evaluated both the in vitro and in vivo effects of suberoylanilide hydroxamic acid (SAHA), an HDAC inhibitor, on EBV‐positive and EBV‐negative T and NK lymphoma cells. Several EBV‐positive and EBV‐negative T and NK cell lines were treated with various concentrations of SAHA. SAHA suppressed the proliferation of T and NK cell lines, although no significant difference was observed between EBV‐positive and EBV‐negative cell lines. SAHA induced apoptosis and/or cell cycle arrest in several T and NK cell lines. In addition, SAHA increased the expression of EBV‐lytic genes and decreased the expression of EBV‐latent genes. Next, EBV‐positive NK cell lymphoma cells were subcutaneously inoculated into severely immunodeficient NOD/Shi‐scid/IL‐2Rγnull mice, and then SAHA was administered intraperitoneally. SAHA inhibited tumor progression and metastasis in the murine xenograft model. 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.
SAHA inhibits tumor growth and metastasis of EBV‐positive NK cell lymphoma. EBER‐positive cells were detected by in situ hybridization in organ tissues of SAHA‐treated or control mice. |
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AbstractList | The ubiquitous Epstein–Barr virus (EBV) infects not only B cells but also T cells and natural killer (NK) cells and is associated with various lymphoid malignancies. Recent studies have reported that histone deacetylase (HDAC) inhibitors exert anticancer effects against various tumor cells. In the present study, we have evaluated both the
in vitro
and
in vivo
effects of suberoylanilide hydroxamic acid (SAHA), an HDAC inhibitor, on EBV-positive and EBV-negative T and NK lymphoma cells. Several EBV-positive and EBV-negative T and NK cell lines were treated with various concentrations of SAHA. SAHA suppressed the proliferation of T and NK cell lines, although no significant difference was observed between EBV-positive and EBV-negative cell lines. SAHA induced apoptosis and/or cell cycle arrest in several T and NK cell lines. In addition, SAHA increased the expression of EBV-lytic genes and decreased the expression of EBV-latent genes. Next, EBV-positive NK cell lymphoma cells were subcutaneously inoculated into severely immunodeficient NOD/Shi-scid/IL-2Rγnull mice, and then SAHA was administered intraperitoneally. SAHA inhibited tumor progression and metastasis in the murine xenograft model. 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. The ubiquitous Epstein-Barr virus (EBV) infects not only B cells but also T cells and natural killer (NK) cells and is associated with various lymphoid malignancies. Recent studies have reported that histone deacetylase (HDAC) inhibitors exert anticancer effects against various tumor cells. In the present study, we have evaluated both the in vitro and in vivo effects of suberoylanilide hydroxamic acid (SAHA), an HDAC inhibitor, on EBV-positive and EBV-negative T and NK lymphoma cells. Several EBV-positive and EBV-negative T and NK cell lines were treated with various concentrations of SAHA. SAHA suppressed the proliferation of T and NK cell lines, although no significant difference was observed between EBV-positive and EBV-negative cell lines. SAHA induced apoptosis and/or cell cycle arrest in several T and NK cell lines. In addition, SAHA increased the expression of EBV-lytic genes and decreased the expression of EBV-latent genes. Next, EBV-positive NK cell lymphoma cells were subcutaneously inoculated into severely immunodeficient NOD/Shi-scid/IL-2Rγnull mice, and then SAHA was administered intraperitoneally. SAHA inhibited tumor progression and metastasis in the murine xenograft model. 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. The ubiquitous Epstein-Barr virus (EBV) infects not only B cells but also T cells and natural killer (NK) cells and is associated with various lymphoid malignancies. Recent studies have reported that histone deacetylase (HDAC) inhibitors exert anticancer effects against various tumor cells. In the present study, we have evaluated both the in vitro and in vivo effects of suberoylanilide hydroxamic acid (SAHA), an HDAC inhibitor, on EBV-positive and EBV-negative T and NK lymphoma cells. Several EBV-positive and EBV-negative T and NK cell lines were treated with various concentrations of SAHA. SAHA suppressed the proliferation of T and NK cell lines, although no significant difference was observed between EBV-positive and EBV-negative cell lines. SAHA induced apoptosis and/or cell cycle arrest in several T and NK cell lines. In addition, SAHA increased the expression of EBV-lytic genes and decreased the expression of EBV-latent genes. Next, EBV-positive NK cell lymphoma cells were subcutaneously inoculated into severely immunodeficient NOD/Shi-scid/IL-2R gamma null mice, and then SAHA was administered intraperitoneally. SAHA inhibited tumor progression and metastasis in the murine xenograft model. 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. SAHA inhibits tumor growth and metastasis of EBV-positive NK cell lymphoma. EBER-positive cells were detected by in situ hybridization in organ tissues of SAHA-treated or control mice. The ubiquitous Epstein–Barr virus (EBV) infects not only B cells but also T cells and natural killer (NK) cells and is associated with various lymphoid malignancies. Recent studies have reported that histone deacetylase (HDAC) inhibitors exert anticancer effects against various tumor cells. In the present study, we have evaluated both the in vitro and in vivo effects of suberoylanilide hydroxamic acid (SAHA), an HDAC inhibitor, on EBV‐positive and EBV‐negative T and NK lymphoma cells. Several EBV‐positive and EBV‐negative T and NK cell lines were treated with various concentrations of SAHA. SAHA suppressed the proliferation of T and NK cell lines, although no significant difference was observed between EBV‐positive and EBV‐negative cell lines. SAHA induced apoptosis and/or cell cycle arrest in several T and NK cell lines. In addition, SAHA increased the expression of EBV‐lytic genes and decreased the expression of EBV‐latent genes. Next, EBV‐positive NK cell lymphoma cells were subcutaneously inoculated into severely immunodeficient NOD/Shi‐scid/IL‐2Rγnull mice, and then SAHA was administered intraperitoneally. SAHA inhibited tumor progression and metastasis in the murine xenograft model. 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. SAHA inhibits tumor growth and metastasis of EBV‐positive NK cell lymphoma. EBER‐positive cells were detected by in situ hybridization in organ tissues of SAHA‐treated or control mice. |
Author | Suzuki, Michio Imadome, Ken‐Ichi Goshima, Fumi Nakagawa, Hikaru Siddiquey, Mohammed N.A. Iwata, Seiko Kanazawa, Tetsuhiro Fujiwara, Shigeyoshi Kimura, Hiroshi Murata, Takayuki |
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BackLink | https://www.ncbi.nlm.nih.gov/pubmed/24712440$$D View this record in MEDLINE/PubMed |
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Copyright | 2014 The Authors. Cancer Science published by Wiley Publishing Asia Pty Ltd on behalf of Japanese Cancer Association. 2014. This work is published under http://creativecommons.org/licenses/by-nc-nd/3.0/ (the “License”). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License. 2014 The Authors. Cancer Science published by Wiley Publishing Asia Pty Ltd on behalf of Japanese Cancer Association. 2014 |
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Keywords | human herpesvirus 4 hydroxamic acid Extranodal NK-T-cell lymphoma SCID mice histone deacetylase inhibitor |
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Snippet | The ubiquitous Epstein–Barr virus (EBV) infects not only B cells but also T cells and natural killer (NK) cells and is associated with various lymphoid... The ubiquitous Epstein-Barr virus (EBV) infects not only B cells but also T cells and natural killer (NK) cells and is associated with various lymphoid... The ubiquitous Epstein–Barr virus ( EBV ) infects not only B cells but also T cells and natural killer ( NK ) cells and is associated with various lymphoid... |
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SubjectTerms | Acids Animals Antineoplastic Agents - therapeutic use Apoptosis Apoptosis - drug effects Cancer Cell cycle Cell Cycle Checkpoints - drug effects Cell Line, Tumor Disease Progression Epstein-Barr virus Epstein-Barr Virus Infections - drug therapy Extranodal NK‐T‐cell lymphoma Female Flow cytometry Gene expression Herpesvirus 4, Human Histone deacetylase histone deacetylase inhibitor Histone Deacetylase Inhibitors - therapeutic use human herpesvirus 4 Humans Hydroxamic acid Hydroxamic Acids - therapeutic use Immunodeficiency Infections Interleukin Receptor Common gamma Subunit - genetics Jurkat Cells Killer Cells, Natural - virology Leukemia Lymphocytes Lymphocytes B Lymphocytes T Lymphoma Lymphoma, T-Cell - drug therapy Lymphoma, T-Cell - virology Metastases Metastasis Mice Mice, Inbred NOD Mice, Knockout Mice, SCID Natural killer cells Neoplasm Metastasis Neoplasm Transplantation Original SCID mice T-Lymphocytes - virology Transplantation, Heterologous Tumor cells Xenograft Model Antitumor Assays Xenografts |
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Title | Anti‐tumor effects of suberoylanilide hydroxamic acid on Epstein–Barr virus‐associated T cell and natural killer cell lymphoma |
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