ArticleFASEB journal : official publication of the Federation of American Societies for Experimental Biology2014
Overexpression of histone deacetylases in cancer cells is controlled by interplay of transcription factors and epigenetic modulators.
Article in FASEB journal : official publication of the Federation of American Societies for Experimental Biology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers.
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Who cites it
43 citing papers in PubMed, 74 citations in OpenAlex.
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- Epigenetic Modifications in Osteosarcoma: Mechanisms and Therapeutic Strategies.Life (Basel, Switzerland) · 2025Review
- The Impact of Tartrazine on DNA Methylation, Histone Deacetylation, and Genomic Stability in Human Cell Lines.Nutrients · 2025Article
- Design, synthesis, biological andBiomedical reports · 2025Article
- The role of short-chain fatty acids in cancer prevention and cancer treatment.Archives of biochemistry and biophysics · 2024Review
- Potential role of short-chain fatty acids in the pathogenesis and management of acute lymphocytic leukemia.Annals of translational medicine · 2024Review
- The epigenetic landscape in intestinal stem cells and its deregulation in colorectal cancer.Stem cells (Dayton, Ohio) · 2024Review
- Mechanisms of the Antineoplastic Effects of New Fluoroquinolones in 2D and 3D Human Breast and Bladder Cancer Cell Lines.Cancers · 2024Article
- Complexation of histone deacetylase inhibitor belinostat to Cu(II) prevents premature metabolic inactivation in vitro and demonstrates potent anti-cancer activity in vitro and ex vivo in colon cancer.Cellular oncology (Dordrecht, Netherlands) · 2024Article
- Platinum(IV) Prodrugs Incorporating an Indole-Based Derivative, 5-Benzyloxyindole-3-Acetic Acid in the Axial Position Exhibit Prominent Anticancer Activity.International journal of molecular sciences · 2024Article
- Epigenetic modifications: Key players in cancer heterogeneity and drug resistance.Translational oncology · 2024Article
- Role of Histone Deacetylase 6 and Histone Deacetylase 6 Inhibition in Colorectal Cancer.Pharmaceutics · 2023Review
- N-terminal domain of classical swine fever virus NJournal of virology · 2023Article
- CREPT Disarms the Inhibitory Activity of HDAC1 on Oncogene Expression to Promote Tumorigenesis.Cancers · 2022Article
- Advances of Epigenetic Biomarkers and Epigenome Editing for Early Diagnosis in Breast Cancer.International journal of molecular sciences · 2022Review
- Unique combinations of epigenetic modifiers synergistically impair the viability of the U87 glioblastoma cell line while exhibiting minor or moderate effects on normal stem cell growth.Medical oncology (Northwood, London, England) · 2022Article
- Towards targeting of shared mechanisms of cancer metastasis and therapy resistance.Nature reviews. Cancer · 2022Review
- Therapeutic potential of tucidinostat, a subtype-selective HDAC inhibitor, in cancer treatment.Frontiers in pharmacology · 2022Review
- Integrated Analysis Reveals the Potential Significance of HDAC Family Genes in Lung Adenocarcinoma.Frontiers in genetics · 2022Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
Histone deacetylases (HDACs) that deacetylate histone and nonhistone proteins play crucial roles in a variety of cellular processes. The overexpression of HDACs is reported in many cancer types and is directly linked to accelerated cell proliferation and survival. However, little is known about how HDAC expression is regulated in cancer cells. In this study, we found that HDAC1 and HDAC2 promoters are regulated through collaborative binding of transcription factors Sp1/Sp3 and epigenetic modulators, including histone H3K4 methyltransferase SET1 and histone acetyltransferase p300, whose levels are also elevated in colon cancer cell lines and patient samples. Interestingly, Sp1 and Sp3 differentially regulate HDAC1 and HDAC2 promoter activity. In addition, Sp1/Sp3 recruits SET1 and p300 to the promoters. SET1 knockdown (KD) results in a loss of the H3K4 trimethylation mark at the promoters, as well as destabilizes p300 at the promoters. Conversely, p300 also influences SET1 recruitment and H3K4me3 level, indicating a crosstalk between p300 and SET1. Further, SET1 KD reduces Sp1 binding to the HDAC1 promoter through the increase of Sp1 acetylation. These results indicate that interactions among transcription factors and epigenetic modulators orchestrate the activation of HDAC1 and HDAC2 promoter activity in colon cancer cells.
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