ArticleCancer science2010
Romidepsin (FK228), a potent histone deacetylase inhibitor, induces apoptosis through the generation of hydrogen peroxide.
Article in Cancer science, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 41 citations in OpenAlex.
- Unlocking the Epigenetic Landscape of Colorectal Cancer: A Step Toward Epigenetics to Precision.Sub-cellular biochemistry · 2026Review
- Epi-revolution in rheumatology: the potential of histone deacetylase inhibitors for targeted rheumatoid arthritis intervention.Inflammopharmacology · 2024Review
- Epigenetic small-molecule screen for inhibition and reversal of acinar ductal metaplasia in mouse pancreatic organoids.Frontiers in pharmacology · 2024Article
- Romidepsin and tamoxifen cooperatively induce senescence of pancreatic cancer cells through downregulation of FOXM1 expression and induction of reactive oxygen species/lipid peroxidation.Molecular biology reports · 2022Article
- Anticancer Therapy with HDAC Inhibitors: Mechanism-Based Combination Strategies and Future Perspectives.Cancers · 2021Review
- Romidepsin (FK228) regulates the expression of the immune checkpoint ligand PD-L1 and suppresses cellular immune functions in colon cancer.Cancer immunology, immunotherapy : CII · 2021Article
- Histone Modifications and their Role in Colorectal Cancer (Review).Pathology oncology research : POR · 2020Review
- Origin and bioactivities of thiosulfinated FK228.MedChemComm · 2019Article
- Combinatorial Antitumor Activity of Oxaliplatin with Epigenetic Modifying Agents, 5-Aza-CdR and FK228, in Human Gastric Cancer Cells.Biomolecules & therapeutics · 2018Article
- The histone deacetylase inhibitor, romidepsin, as a potential treatment for pulmonary fibrosis.Oncotarget · 2017Article
- Inhibitors of Histone Deacetylases Are Weak Activators of theBioMed research international · 2017Article
- Crosstalk among the proteome, lysine phosphorylation, and acetylation in romidepsin-treated colon cancer cells.Oncotarget · 2016Article
- Romidepsin enhances the cytotoxicity of fludarabine, clofarabine and busulfan combination in malignant T-cells.Leukemia research · 2016Article
- Multi-walled carbon nanotube induces nitrative DNA damage in human lung epithelial cells via HMGB1-RAGE interaction and Toll-like receptor 9 activation.Particle and fibre toxicology · 2016Article
- Treating Colon Cancer Cells with FK228 Reveals a Link between Histone Lysine Acetylation and Extensive Changes in the Cellular Proteome.Scientific reports · 2015Article
- Romidepsin targets multiple survival signaling pathways in malignant T cells.Blood cancer journal · 2015Article
- Histone deacetylases as targets for treatment of multiple diseases.Clinical science (London, England : 1979) · 2013Review
- Oxidative stress and lipid peroxidation products in cancer progression and therapy.ISRN oncology · 2012Article
Corrections and comments
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Authors and funding
9 authors at 5 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Romidepsin (FK228) is a potent histone deacetylase (HDAC) inhibitor, which has a potent anticancer activity, but its molecular mechanism is unknown. We investigated the mechanism of FK228-induced apoptosis in the human leukemia cell line HL-60 and its hydrogen peroxide (H(2)O(2))-resistant sub-clone, HP100, and the human colon cancer cell line Caco-2. Cytotoxicity and DNA ladder formation induced by FK228 could be detected in HL-60 cells after a 24-h incubation, whereas they could not be detected in HP100 cells. Trichostatin A (TSA), an HDAC inhibitor, induced DNA ladder formation in both HL-60 and HP100 cells. In contrast, FK228 inhibited HDAC activity in both HL-60 and HP100 cells to a similar extent. These findings suggest that FK228-induced apoptosis involves H(2)O(2)-mediated pathways and that TSA-induced apoptosis does not. Flow cytometry revealed H(2)O(2) formation and a change in mitochondrial membrane potential (Δψm) in FK228-treated cells. FK228 also induced apoptosis in Caco-2 cells, which was prevented by N-acetyl-cysteine, suggesting that reactive oxygen species participate in apoptosis in various types of tumor cells. Interestingly, in a cell-free system, FK228 generated superoxide (O(2)(-)) in the presence of glutathione, suggesting that H(2)O(2) is derived from dismutation of O(2)(-) produced through redox-cycle of FK228. Therefore, in addition to HDAC inhibition, H(2)O(2) generated from FK228 may participate in its apoptotic effect.
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