ArticleBMC biochemistry2015
Histone deacetylase inhibitor sodium butyrate suppresses DNA double strand break repair induced by etoposide more effectively in MCF-7 cells than in HEK293 cells.
Article in BMC biochemistry, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.
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33 citing papers in PubMed, 54 citations in OpenAlex.
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- Investigating dynamics of lentiviral vector secretion from HEK293T producer cells using a fractionated perfusion system.Biotechnology journal · 2024Article
- Uncovering a novel mechanism: Butyrate induces estrogen receptor alpha activation independent of estrogen stimulation in MCF-7 breast cancer cells.Genetics and molecular biology · 2024Article
- Mechanistic Insights into the Anti-Proliferative Action of Gut Microbial Metabolites against Breast Adenocarcinoma Cells.International journal of molecular sciences · 2023Article
- Histone deacetylase inhibitors promote breast cancer metastasis by elevating NEDD9 expression.Signal transduction and targeted therapy · 2023Article
- Short chain fatty acids prime colorectal cancer cells to activate antitumor immunity.Frontiers in immunology · 2023Article
- Gut Metabolites and Breast Cancer: The Continuum of Dysbiosis, Breast Cancer Risk, and Potential Breast Cancer Therapy.International journal of molecular sciences · 2022Review
- HDAC Inhibitor Sodium Butyrate Attenuates the DNA Repair in Transformed but Not in Normal Fibroblasts.International journal of molecular sciences · 2022Article
- Epigenetic Factors as Etiological Agents, Diagnostic Markers, and Therapeutic Targets for Luminal Breast Cancer.Biomedicines · 2022Review
- Evaluation of the antioxidative and genotoxic effects of sodium butyrate on breast cancer cells.Saudi journal of biological sciences · 2022Article
- Short chain fatty acids exhibit selective estrogen receptor downregulator (SERD) activity in breast cancer.American journal of cancer research · 2022Article
- Consumption of Dairy Products and the Risk of Developing Breast Cancer in Polish Women.Nutrients · 2021Article
- Development and validation of the TGx-HDACi transcriptomic biomarker to detect histone deacetylase inhibitors in human TK6 cells.Archives of toxicology · 2021Article
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundHistone deacetylase inhibitors (HDACi's) are emerging as promising anticancer drugs alone or in combination with chemotherapy or radiotherapy agents. Previous research suggests that HDACi's have a high degree of selectivity for killing cancer cells, but little is known regarding the impact of different cellular contexts on HDACi treatment. It is likely that the molecular mechanisms of HDACi's involve processes that depend on the chromatin template, such as DNA damage and repair. We sought to establish the connection between the HDACi sodium butyrate and DNA double-strand break (DSB) damage in human breast cancer MCF-7 and non-cancerous human embryonic kidney293 (HEK293) cells.
resultsSodium butyrate inhibited the proliferation of both HEK293 and MCF-7 cells in a dose- and time- dependent manner, but the effects on MCF-7 cells were more obvious. This differential effect on cell growth was not explained by differences in cell cycle arrest, as sodium butyrate caused an arrest in G1/G2 phase and a decrease in S phase for both cell lines. At high doses of sodium butyrate or in combination with etoposide, MCF-7 cells formed fewer colonies than HEK293 cells. Furthermore, sodium butyrate enhanced the formation of etoposide-induced γ-H2AX foci to a greater extent in MCF-7 than in HEK293 cells. The two cells also displayed differential patterns in the nuclear expression of DNA DSB repair proteins, which could, in part, explain the cytotoxic effects of sodium butyrate.
conclusionsThese studies suggest that sodium butyrate treatment leads to a different degree of chromatin relaxation in HEK293 and cancerous MCF-7 cells, which results in differential sensitivity to the toxic effects of etoposide in controlling damaged DNA repair.
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