ArticleJournal of cancer research and clinical oncology2024
Butyrate inhibits the malignant biological behaviors of breast cancer cells by facilitating cuproptosis-associated gene expression.
Article in Journal of cancer research and clinical oncology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers, 1 of them a synthesis that pooled it.
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Who cites it
16 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Cuproptosis as a therapeutic target in cancer: a Systematic Review and bibliometric analysis of the research landscape.Frontiers in oncology · 2025Pooled it
- The neuroimmune axis in breast cancer: from mechanistic insights to clinical applications.BMC medicine · 2026Review
- Differences in composition and diversity of the gut microbiota of post-menopausal breast cancer patients.Scientific reports · 2026Article
- Remodeling the tumor immune microenvironment: mechanisms of crosstalk between regulated cell death macrophages.Frontiers in immunology · 2026Review
- Role of Copper Homeostasis and Cuproptosis in Cardiovascular Disease: Molecular Insights and Metabolic Perspectives.International journal of biological sciences · 2026Review
- Identification of molecular subtypes for breast cancer based on butyrate metabolism-related genes to assess prognosis and immune landscape.Translational cancer research · 2025Article
- Copper Homeostasis and Cuproptosis As Potential Intervention Strategy in Atherosclerosis.Journal of cardiovascular translational research · 2025Review
- Long-Term Breastfeeding: Protective Effects Against Triple-Negative Breast Cancer and the Role of the Breast Microbiota.Pathogens (Basel, Switzerland) · 2025Review
- Targeting cuproptosis for cancer therapy: Focus on the anti-tumor immune system.Cancer pathogenesis and therapy · 2025Review
- The butyrate derived from probiotic Clostridium butyricum exhibits an inhibitory effect on multiple myeloma through cell death induction.Scientific reports · 2025Article
- Gut dysbiosis conveys psychological stress to activate LRP5/β-catenin pathway promoting cancer stemness.Signal transduction and targeted therapy · 2025Article
- Gut-Brain-Microbiome Axis in the Regulation of Cancer Immune Escape and Immunotherapy in Tumors.Research (Washington, D.C.) · 2025Review
- Sodium butyrate and sodium propionate inhibit breast cancer cell migration and invasion through regulation of epithelial-to-mesenchymal transition and suppression of MEK/ERK signaling pathway.Frontiers in cell and developmental biology · 2025Article
- Emerging Role of Gut Microbiota in Breast Cancer Development and Its Implications in Treatment.Metabolites · 2024Review
- The Link Between the Gut Microbiome and Bone Metastasis.International journal of molecular sciences · 2024Review
- Elucidating the evolving role of cuproptosis in breast cancer progression.International journal of biological sciences · 2024Review
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Authors and funding
3 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundButyrate is a common short-chain fatty acids (SCFA), and it has been demonstrated to regulate the development of breast cancer (BC), while the underlying mechanism is still unreported.
methodsGas chromatography was used to measure the amounts of SCFA (acetate, propionate, and butyrate) in the feces. Cell viability was measured by the CCK-8 assay. The wound healing assay demonstrated cell migration, and the transwell assay demonstrated cell invasion. The levels of protein and gene were determined by western blot assay and RT-qPCR assay, respectively.
resultsThe levels of SCFA were lower in the faecal samples from BC patients compared to control samples. In cellular experiments, butyrate significantly suppressed the cell viability, migration and invasion of T47D in a dose-dependent manner. In animal experiments, butyrate effectively impeded the growth of BC tumors. Toll like receptor 4 (TLR4) was highly expressed in the tumors from BC patients. Butyrate inhibited the expression of TLR4. In addition, butyrate promoted the expression of cuproptosis-related genes including PDXK (pyridoxal kinase) and SLC25A28 (solute carrier family 25 member 28), which was lowly expressed in BC tumors. Importantly, overexpression of TLR4 can reverses the promotion of butyrate to PDXK and SLC25A28 expression and the prevention of butyrate to the malignant biological behaviors of T47D cells.
conclusionIn summary, butyrate inhibits the development of BC by facilitating the expression of PDXK and SLC25A28 through inhibition of TLR4. Our investigation first identified a connection among butyrate, TLR4 and cuproptosis-related genes in BC progression. These findings may provide novel target for the treatment of BC.
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