ArticleMitochondrion2014
Sodium butyrate induces DRP1-mediated mitochondrial fusion and apoptosis in human colorectal cancer cells.
Article in Mitochondrion, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 56 papers.
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Who cites it
56 citing papers in PubMed, 97 citations in OpenAlex.
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- Targeting mitochondria as a potential therapeutic strategy against radioresistance in cancer.Frontiers in oncology · 2026Review
- The role of mitochondria-endoplasmic reticulum crosstalk in colorectal cancer.Genes & diseases · 2026Review
- Sodium butyrate-induced autophagy in colorectal cancer unveils the Ca²⁺/CaMKKβ signaling pathway as a potential therapeutic target.Scientific reports · 2025Article
- The role of mitochondrial biogenesis, mitochondrial dynamics and mitophagy in gastrointestinal tumors.Cancer cell international · 2025Review
- Construction of a novel mitochondrial oxidative stress-related genes prognostic system and molecular subtype characterization for breast cancer.Discover oncology · 2024Article
- Antioxidant Role of Probiotics in Inflammation-Induced Colorectal Cancer.International journal of molecular sciences · 2024Review
- Novel therapeutic targets: bifidobacterium-mediated urea cycle regulation in colorectal cancer.Cell biology and toxicology · 2024Article
- Drp1: Focus on Diseases Triggered by the Mitochondrial Pathway.Cell biochemistry and biophysics · 2024Review
- Mitochondrial fusion-fission dynamics and its involvement in colorectal cancer.Molecular oncology · 2024Review
- Mitochondrial dynamics and colorectal cancer biology: mechanisms and potential targets.Cell communication and signaling : CCS · 2024Review
- Sodium Butyrate Inhibits the Expression of Thymidylate Synthase and Induces Cell Death in Colorectal Cancer Cells.International journal of molecular sciences · 2024Article
- Diallyl Trisulfide Induces ROS-Mediated Mitotic Arrest and Apoptosis and Inhibits HNSCC Tumor Growth and Cancer Stemness.Cancers · 2024Article
- Nutrigenomic underpinnings of intestinal stem cells in inflammatory bowel disease and colorectal cancer development.Frontiers in genetics · 2024Review
- Mitochondria: a crucial factor in the progression and drug resistance of colorectal cancer.Frontiers in immunology · 2024Review
- Targeting CDK1 in cancer: mechanisms and implications.NPJ precision oncology · 2023Review
- Control of Redox Homeostasis by Short-Chain Fatty Acids: Implications for the Prevention and Treatment of Breast Cancer.Pathogens (Basel, Switzerland) · 2023Review
- Integrative analysis of circadian clock with prognostic and immunological biomarker identification in ovarian cancer.Frontiers in molecular biosciences · 2023Article
- Functional high-throughput screen identifies microRNAs that promote butyrate-induced death in colorectal cancer cells.Molecular therapy. Nucleic acids · 2022Article
- Mitochondrial Control in Inflammatory Gastrointestinal Diseases.International journal of molecular sciences · 2022Review
Corrections and comments
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Authors and funding
5 authors at 3 institutions in 2 countries.
Funding
Abstract
Sodium butyrate (NaBt) is the byproduct of anaerobic microbial fermentation inside the gastro-intestinal tract that could reach up to 20mM, and has been shown to inhibit the growth of various cancers. Herein, we evaluated its effect on mitochondrial fusion and associated induction of apoptosis in colorectal cancer cells (CRC). NaBt treatment at physiological (1-5mM) concentrations for 12 and 24h decreased the cell viability and induced G2-M phase cell cycle arrest in HCT116 (12h) and SW480 human CRC cells. This cell cycle arrest was associated with mitochondria-mediated apoptosis accompanied by a decrease in survivin and Bcl-2 expression, and generation of reactive oxygen species (ROS). Furthermore, NaBt treatment resulted in a significant decrease in the mitochondrial mass which is an indicator of mitochondrial fusion. Level of dynamin-related protein 1 (DRP1), a key regulator of mitochondrial fission and fusion where its up-regulation correlates with fission, was found to be decreased in CRC cells. Further, at early treatment time, DRP1 down-regulation was noticed in mitochondria which later became drastically reduced in both mitochondria as well as cytosol. DRP1 is activated by cyclin B1-CDK1 complex by its ser616 phosphorylation in which both cyclin B1-CDK1 complex and phospho-DRP1 (ser616) were strongly reduced by NaBt treatment. DRP1 was observed to be regulated by apoptosis as pan-caspase inhibitor showing rescue from NaBt-induced apoptosis also caused the reversal of DRP1 to the normal level as in control proliferating cells. Together, these findings suggest that NaBt can modulate mitochondrial fission and fusion by regulating the level of DRP1 and induce cell cycle arrest and apoptosis in human CRC cells.
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