ArticleBritish journal of pharmacology2002
Sodium butyrate induces P53-independent, Fas-mediated apoptosis in MCF-7 human breast cancer cells.
Article in British journal of pharmacology, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.
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Who cites it
37 citing papers in PubMed, 101 citations in OpenAlex.
- Molecular mechanisms involved in the anticancer activities of probiotics and postbiotics.Cancer cell international · 2026Review
- Integrative mendelian randomization and multi-omics analysis reveal a gut microbiota-metabolite-CXCL10 axis in breast cancer.AMB Express · 2025Article
- Bacterial metabolites: Effects on the development of breast cancer and therapeutic efficacy (Review).Oncology letters · 2025Review
- Insights into the gut microbiome-metabolite dynamics in breast cancer.Gut microbes reports · 2025Review
- Article
- The PRC2 complex epigenetically silences GATA4 to suppress cellular senescence and promote the progression of breast cancer.Translational oncology · 2024Article
- Cytotoxic Potential of Betulinic Acid Fatty Esters and Their Liposomal Formulations: Targeting Breast, Colon, and Lung Cancer Cell Lines.Molecules (Basel, Switzerland) · 2024Article
- Mechanistic Insights into the Anti-Proliferative Action of Gut Microbial Metabolites against Breast Adenocarcinoma Cells.International journal of molecular sciences · 2023Article
- Sodium butyrate supresses malignant human mast cell proliferation, downregulates expression of KIT and promotes differentiation.Frontiers in allergy · 2023Article
- Gut Metabolites and Breast Cancer: The Continuum of Dysbiosis, Breast Cancer Risk, and Potential Breast Cancer Therapy.International journal of molecular sciences · 2022Review
- Bladder cancer, inflammageing and microbiomes.Nature reviews. Urology · 2022Review
- Effect of Sodium Butyrate on p16INK4a, p14ARF, p15INK4b, Class I HDACs (HDACs 1, 2, 3) Class II HDACs (HDACs 4, 5, 6), Cell Growth Inhibition and Apoptosis Induction in Pancreatic Cancer AsPC-1 and Colon Cancer HCT-116 Cell Lines.Asian Pacific journal of cancer prevention : APJCP · 2022Article
- Potential of histone deacetylase inhibitors in the control and regulation of prostate, breast and ovarian cancer.Frontiers in chemistry · 2022Review
- Fecal microbiota transplantation as a new treatment for canine inflammatory bowel disease.Bioscience of microbiota, food and health · 2021Article
- High-Throughput Quantitative Top-Down Proteomics: Histone H4.Journal of the American Society for Mass Spectrometry · 2019Article
- Effects of Intestinal Microbial⁻Elaborated Butyrate on Oncogenic Signaling Pathways.Nutrients · 2019Review
- Impact of Different Types of Diet on Gut Microbiota Profiles and Cancer Prevention and Treatment.Medicina (Kaunas, Lithuania) · 2019Review
- Article
- TXNIP mediates the differential responses of A549 cells to sodium butyrate and sodium 4-phenylbutyrate treatment.Cancer medicine · 2017Article
- Phenylbutyrate-a pan-HDAC inhibitor-suppresses proliferation of glioblastoma LN-229 cell line.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2016Article
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
1. This study was performed to determine the effect and action mechanisms of sodium butyrate (NaB) on the growth of breast cancer cells. 2. Butyrate inhibited the growth of all breast cancer cell lines analysed. It induced cell cycle arrest in G1 and apoptosis in MCF-7, MCF-7ras, T47-D, and BT-20 cells, as well as arrest in G2/M in MDA-MB-231 cells. 3. Transient transfection of MCF-7 and T47-D cells with wild-type and antisense p53 did not modify butyrate-induced apoptosis. Pifithrin-alpha, which inhibits the transcriptional activity of P53, did not modify cell growth or apoptosis of MCF-7 and T47-D cells treated with butyrate. These results indicate that P53 was not involved in butyrate-induced growth inhibition of breast cancer cells. 4. Treatment of MCF-7 cells with anti-Fas agonist antibody induced cell death, indicating that Fas was functional in these cells. Moreover, butyrate potentiated Fas-induced apoptosis, as massive apoptosis was observed rapidly when MCF-7 cells were treated with butyrate and anti-Fas agonist antibody. In addition, butyrate-induced apoptosis in MCF-7 cells was considerably reduced by anti-Fas antagonist antibody. Western blot analysis showed that butyrate increased Fas and Fas ligand levels (Fas L), indicating that butyrate-induced apoptosis may be mediated by Fas signalling. 5. These results demonstrate that butyrate inhibited the growth of breast cancer cells in a P53-independent manner. Moreover, it induced apoptosis via the Fas/Fas L system and potentiated Fas-triggered apoptosis in MCF-7 cells. These findings may open interesting perspectives in human breast cancer treatment strategy.
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