ArticleFrontiers in allergy2023
Sodium butyrate supresses malignant human mast cell proliferation, downregulates expression of KIT and promotes differentiation.
Article in Frontiers in allergy, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed, 8 citations in OpenAlex.
- Microbial short chain fatty acids: Effective histone deacetylase inhibitors in immune regulation (Review).International journal of molecular medicine · 2026Review
- Butyrate Selectively Targets Super-Enhancers and Transcriptional Networks Associated with Human Mast Cell Function.European journal of immunology · 2025Article
- Article
- Overview of the immunological mechanisms in hepatitis B virus reactivation: Implications for disease progression and management strategies.World journal of gastroenterology · 2024Review
- Genetic Changes in Mastocytes and Their Significance in Mast Cell Tumor Prognosis and Treatment.Genes · 2024Review
- Epigenetic histone modification by butyrate downregulates KIT and attenuates mast cell function.Journal of cellular and molecular medicine · 2023Article
Corrections and comments
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Authors and funding
4 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Sodium butyrate (NaBu) is a class I histone deacetylase inhibitor (HDACi) that can impede the proliferation of transformed cells. Although some HDACi downregulate the expression of the stem cell factor receptor (KIT/CD117), the effect of NaBu on KIT expression and human mast cell proliferation requires further elucidation. In this study, we examined the effects of NaBu on three transformed human mast cell lines, HMC-1.1, HMC-1.2 and LAD2. NaBu (100 µM) inhibited the proliferation and metabolic activity of all three cell lines without significantly affecting their viability, suggesting that although the cells had ceased to divide, they were not yet undergoing apoptosis. Cell cycle analysis using the cell-permeant dye, propidium iodide, indicated that NaBu significantly blocked the cell cycle progression of HMC-1.1 and HMC-1.2 from G1 to G2/M phases. Furthermore, NaBu downregulated the expression of
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Registered trials
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