Tubacin Kills Epstein-Barr Virus (EBV)-Burkitt Lymphoma Cells by Inducing Reactive Oxygen Species and EBV Lymphoblastoid Cells by Inducing Apoptosis
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Tubacin is a small molecule inhibitor of histone deacetylase 6 and blocks aggresome activity. We found that Epstein-Barr virus (EBV)-positive Burkitt lymphoma (BL) cells were generally killed by lower doses of tubacin than EBV-transformed lymphoblastoid cells (LCLs) or EBV-negative BL cells. Tubacin induced apoptosis of LCLs, which was inhibited by pretreatment with a pancaspase inhibitor but not by butylated hydroxyanisole, which inhibits reactive oxygen species. In contrast, tubacin killed EBV-positive BL cells in a caspase-3-independent pathway that involved reactive oxygen species and was blocked by butylated hydroxyanisole. Previously, we showed that bortezomib, a proteasome inhibitor, induces apoptosis of EBV LCLs and that LCLs are killed by lower doses of bortezomib than EBV-positive BL cells. Here we found that the combination of bortezomib and tubacin acted in synergy to kill EBV-positive BL cells and LCLs. Tubacin or the combination of bortezomib and tubacin did not induce EBV lytic replication. These findings suggest that the combination of a proteasome inhibitor and an HDAC6 inhibitor may represent a useful strategy for the treatment of certain EBV-associated B cell lymphomas.
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HDAC6 has recently emerged as an attractive target for the treatment of cancer.
“HDAC6 has recently emerged as an attractive target for the treatment of cancer (Boyault et al, 2007; Lee et al, 2008; Kawada et al, 2009; Rivieccio et al, 2009).”
From A novel small molecule hydroxamate preferentially inhibits HDAC6 activity and tumour growth (2013) · cites this paper as Kawada et al, 2009
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- Authors
- Kawada, J., Zou, P., Mazitschek, R., Bradner, J. E., & Cohen, J. I.
- Affiliations
- National Institutes of Health (US)
- Broad Institute (US)
- Corresponding author
- Cohen, Jeffrey I.
- Venue
- Journal of Biological Chemistry
- Publisher
- Elsevier BV
- Published
- 2009-06
- Volume
- 284
- Issue
- 25
- Pages
- 17102-17109
- ISSN
- 0021-9258 (ISSN-L)
- PMC
- PMC2719348
- OpenAlex
- W2071380029
- Cited by
- 43
- References
- 35
- Citations by year
- 2025: 3 · 2024: 1 · 2023: 2 · 2020: 1 · 2019: 1 · 2018: 3 · 2017: 2 · 2016: 1 · 2015: 4 · 2014: 4 · 2013: 5 · 2012: 4
- FWCI
- 2.66
- Type
- journal article
- Language
- en
- Open access
- hybrid
- doi.org
- Licence
- Locations
- Journal of Biological Chemistry (publishedVersion, cc-by)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Institutes of Health
- National Cancer Institute (K08CA128972, P01CA078048)
- National Institute of Allergy and Infectious Diseases
- Topics
- Health Sciences › Medicine › Oncology › Viral-associated cancers and disorders
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Histone Deacetylase Inhibitors Research
- Health Sciences › Medicine › Pathology and Forensic Medicine › Lymphoma Diagnosis and Treatment
- Keywords
- tubacin, Epstein-Barr virus, Burkitt lymphoma, reactive oxygen species, apoptosis, bortezomib, proteasome inhibitors, combination therapy, aggresomes
- MeSH terms
- Bortezomib, Histone Deacetylase 6, Anilides, B-Lymphocytes, Boronic Acids, Burkitt Lymphoma, Cell Transformation, Viral, Drug Synergism, Enzyme Inhibitors, Herpesvirus 4, Human, Genes, Viral, Histone Deacetylases, Humans, Hydroxamic Acids, Protease Inhibitors, Pyrazines, Apoptosis, Reactive Oxygen Species, Cell Line, Tumor, Caspase 3, Histone Deacetylase Inhibitors
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