Plasma cell dependence on histone/protein deacetylase 11 reveals a therapeutic target in multiple myeloma
Open accessAbstract
The clinical utility of histone/protein deacetylase (HDAC) inhibitors in combinatorial regimens with proteasome inhibitors for patients with relapsed and refractory multiple myeloma (MM) is often limited by excessive toxicity due to HDAC inhibitor promiscuity with multiple HDACs. Therefore, more selective inhibition minimizing off-target toxicity may increase the clinical effectiveness of HDAC inhibitors. We demonstrated that plasma cell development and survival are dependent upon HDAC11, suggesting this enzyme is a promising therapeutic target in MM. Mice lacking HDAC11 exhibited markedly decreased plasma cell numbers. Accordingly, in vitro plasma cell differentiation was arrested in B cells lacking functional HDAC11. Mechanistically, we showed that HDAC11 is involved in the deacetylation of IRF4 at lysine103. Further, targeting HDAC11 led to IRF4 hyperacetylation, resulting in impaired IRF4 nuclear localization and target promoter binding. Importantly, transient HDAC11 knockdown or treatment with elevenostat, an HDAC11-selective inhibitor, induced cell death in MM cell lines. Elevenostat produced similar anti-MM activity in vivo, improving survival among mice inoculated with 5TGM1 MM cells. Elevenostat demonstrated nanomolar ex vivo activity in 34 MM patient specimens and synergistic activity when combined with bortezomib. Collectively, our data indicated that HDAC11 regulates an essential pathway in plasma cell biology establishing its potential as an emerging theraputic vulnerability in MM.
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Treatment of MM cells with elevenostan induces apoptosis similar to downregulation of HDAC11.
“As a result, treatment of MM cells with elevenostan, a hydroxamic acid derivative and putative selective HDAC11 inhibitor (Fig. 3), induces apoptosis similar to downregulation of HDAC11.”
From HDACs and the epigenetic plasticity of cancer cells: target the complexity (2022) · cites this paper as Mostofa et al., 2021
In MM, HDAC11 regulates cell proliferation and survival by controlling IRF4 acetylation.
“In MM, HDAC11 regulates cell proliferation and survival by controlling IRF4 acetylation.”
From HDACs and the epigenetic plasticity of cancer cells: target the complexity (2022) · cites this paper as Mostofa et al., 2021
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HDACs and the epigenetic plasticity of cancer cells: target the complexity
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- Authors
- Mostofa, A., Distler, A., Meads, M. B., Sahakian, E., Powers, J. J., Achille, A., Noyes, D., Wright, G., Fang, B., Izumi, V., Koomen, J., Rampakrishnan, R., Nguyen, T. P., De Avila, G., Silva, A. S., Sudalagunta, P., Canevarolo, R. R., Siqueira Silva, M. D. C., Alugubelli, R. R., Dai, H. A., Kulkarni, A., Dalton, W. S., Hampton, O. A., Welsh, E. A., Teer, J. K., Tungesvik, A., Wright, K. L., Pinilla-Ibarz, J., Sotomayor, E. M., Shain, K. H., & Brayer, J.
- Affiliations
- Immunology Program,
- Department of Malignant Hematology,
- Proteomics & Metabolomics Core Facility, and
- Chemical Biology and Molecular Medicine Program,
- Moffitt Cancer Center (US)
- Department of Cancer Physiology, Moffitt Cancer Center & Research Institute, Tampa, Florida, USA.
- George Washington University (US)
- M2Gen, Tampa, Florida, USA.
- Corresponding author
- Brayer, Jason
- ORCID
- Mostofa, AGM
- Meads, Mark B.
- Sahakian, Eva
- Powers, John J.
- Wright, Gabriela
- Fang, Bin
- Izumi, Victoria
- Koomen, John
- Silva, Ariosto S.
- Sudalagunta, Praneeth
- Canevarolo, Rafael Renatino
- Alugubelli, Raghunandan Reddy
- Dai, Hongyue A.
- Kulkarni, Amit
- Dalton, William S.
- Hampton, Oliver A.
- Welsh, Eric A.
- Teer, Jamie K.
- Tungesvik, Alexandre
- Wright, Kenneth L.
- Pinilla-Ibarz, Javier
- Sotomayor, Eduardo M.
- Shain, Kenneth H.
- Brayer, Jason
- Venue
- JCI Insight
- Published
- 2021-12-22
- Volume
- 6
- Issue
- 24
- ISSN
- 2379-3708 (ISSN-L)
- PMC
- PMC8783683
- OpenAlex
- W3214304478
- Cited by
- 27
- References
- 68
- Citations by year
- 2026: 9 · 2025: 7 · 2024: 2 · 2023: 2 · 2022: 7
- FWCI
- 1.80
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Licence
- Locations
- JCI Insight (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
- Funders
- H. Lee Moffitt Cancer Center and Research Institute (N/A)
- Topics
- Health Sciences › Medicine › Hematology › Multiple Myeloma Research and Treatments
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Histone Deacetylase Inhibitors Research
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Genomics and Chromatin Dynamics
- Keywords
- HDAC11, multiple myeloma, plasma cells, IRF4, histone deacetylase inhibitors, plasma cell differentiation, bortezomib combination therapy, therapeutic target
- MeSH terms
- Animals, Histones, Humans, Multiple Myeloma, Plasma Cells, Mice, Histone Deacetylase Inhibitors
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
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