Identification of a cancer stem cell-specific function for the histone deacetylases, HDAC1 and HDAC7, in breast and ovarian cancer
Open accessAbstract
Tumours are comprised of a highly heterogeneous population of cells, of which only a small subset of stem-like cells possess the ability to regenerate tumours in vivo. These cancer stem cells (CSCs) represent a significant clinical challenge as they are resistant to conventional cancer therapies and play essential roles in metastasis and tumour relapse. Despite this realization and great interest in CSCs, it has been difficult to develop CSC-targeted treatments due to our limited understanding of CSC biology. Here, we present evidence that specific histone deacetylases (HDACs) play essential roles in the CSC phenotype. Utilizing a novel CSC model, we discovered that the HDACs, HDAC1 and HDAC7, are specifically over-expressed in CSCs when compared to non-stem-tumour-cells (nsTCs). Furthermore, we determine that HDAC1 and HDAC7 are necessary to maintain CSCs, and that over-expression of HDAC7 is sufficient to augment the CSC phenotype. We also demonstrate that clinically available HDAC inhibitors (HDACi) targeting HDAC1 and HDAC7 can be used to preferentially target CSCs. These results provide actionable insights that can be rapidly translated into CSC-specific therapies.
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HDAC7 levels are downregulated after treatment with pan-HDACIs.
“Interestingly, HDAC7 levels are downregulated after treatment with pan-HDACIs (Minisini et al., 2022;Witt et al., 2017).”
From HDACs and the epigenetic plasticity of cancer cells: target the complexity (2022) · cites this paper as Witt et al., 2017
HDAC7 has emerged as a regulator of cancer stem cells.
“In the past few years HDAC7 has emerged as a regulator of cancer stem cells (CSCs).”
From HDACs and the epigenetic plasticity of cancer cells: target the complexity (2022) · cites this paper as Witt et al., 2017
In breast and ovarian cancers, HDAC1 and HDAC7 are specifically overexpressed in CSCs compared to non-stem-tumour cells.
“In breast and ovarian cancers, HDAC1 and HDAC7 are specifically overexpressed in CSCs compared to non-stem-tumourcells.”
From HDACs and the epigenetic plasticity of cancer cells: target the complexity (2022) · cites this paper as Witt et al., 2017
HDAC1 and HDAC7 are necessary to maintain the properties of CSCs.
“HDAC1 and HDAC7 are necessary to maintain the properties of CSCs, and HDAC7 overexpression is sufficient to increase the CSC phenotype (Witt et al., 2017).”
From HDACs and the epigenetic plasticity of cancer cells: target the complexity (2022) · cites this paper as Witt et al., 2017
HDAC7 overexpression is sufficient to increase the CSC phenotype.
“HDAC1 and HDAC7 are necessary to maintain the properties of CSCs, and HDAC7 overexpression is sufficient to increase the CSC phenotype (Witt et al., 2017).”
From HDACs and the epigenetic plasticity of cancer cells: target the complexity (2022) · cites this paper as Witt et al., 2017
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- Authors
- Witt, A. E., Lee, C.-W., Lee, T. I., Azzam, D. J., Wang, B., Caslini, C., Petrocca, F., Grosso, J., Jones, M., Cohick, E. B., Gropper, A. B., Wahlestedt, C., Richardson, A. L., Shiekhattar, R., Young, R. A., & Ince, T. A.
- Affiliations
- University of Miami (US)
- Brigham and Women's Hospital (US)
- Whitehead Institute for Biomedical Research (US)
- Boston Children's Hospital (US)
- Corresponding author
- Ince, T A
- ORCID
- Venue
- Oncogene
- Published
- 2016-10-03
- Volume
- 36
- Issue
- 12
- Pages
- 1707-1720
- ISSN
- 0950-9232 (ISSN-L)
- 1476-5594
- PMC
- PMC5364039
- OpenAlex
- W2527902762
- Cited by
- 172
- References
- 61
- Citations by year
- 2026: 4 · 2025: 9 · 2024: 22 · 2023: 15 · 2022: 32 · 2021: 22 · 2020: 17 · 2019: 17 · 2018: 21 · 2017: 11 · 2016: 1 · 2015: 1
- FWCI
- 8.98
- Type
- journal article
- Language
- en
- Open access
- hybrid
- doi.org
- Licence
- Locations
- Oncogene (publishedVersion, cc-by-nc-nd)
- PubMed Central (publishedVersion, cc-by-nc-nd)
- PubMed (publishedVersion)
- Digital Access to Scholarship at Harvard (DASH) (Harvard University) (submittedVersion, cc-by)
- DSpace@MIT (Massachusetts Institute of Technology) (submittedVersion, cc-by-nc-nd)
- Nature
- Funders
- Breast Cancer Research Foundation
- University of Miami
- Sylvester Comprehensive Cancer Center, University of Miami Health Systems
- Leonard M. Miller School of Medicine
- Leonard M. Miller School of Medicine, University of Miami
- National Cancer Institute (CA146445, R01CA146445, K22CA184244, P30CA010815)
- National Institute of General Medical Sciences (R01GM105754, R01GM078455)
- Congressionally Directed Medical Research Programs (W81XWH-14-1-0160)
- Topics
- Health Sciences › Medicine › Oncology › Cancer Cells and Metastasis
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Histone Deacetylase Inhibitors Research
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Epigenetics and DNA Methylation
- Keywords
- cancer stem cells, histone deacetylase, HDAC1, HDAC7, breast cancer, ovarian cancer, histone deacetylase inhibitors, tumor heterogeneity, CSC-targeted therapy
- MeSH terms
- Animals, Breast Neoplasms, Disease Models, Animal, Female, Genes, Lethal, Histone Deacetylases, Humans, Ovarian Neoplasms, Phenotype, Neoplastic Stem Cells, Biomarkers, RNA, Small Interfering, Cell Line, Tumor, Mice, Gene Knockdown Techniques, Drug Discovery, Histone Deacetylase 1, Histone Deacetylase Inhibitors, Heterografts
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