ArticleInternational journal of molecular sciences2024
Sodium Butyrate Inhibits the Expression of Thymidylate Synthase and Induces Cell Death in Colorectal Cancer Cells.
Article in International journal of molecular sciences, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 10 citations in OpenAlex.
- Developing Anticancer Redox Chemotherapeutics: Challenges and Opportunities.Oral diseases · 2026Article
- Sodium butyrate suppresses endometrial cancer cell growth by inhibiting thymidylate synthase and reprogramming pyrimidine metabolism.Genes & nutrition · 2026Article
- Uncovering a novel treatment strategy: sodium butyrate overcomes cisplatin resistance in the oral squamous cell carcinoma by inducing ferroptosis.Journal of experimental & clinical cancer research : CR · 2026Article
- Gut microbiota-mediated chemotherapy resistance in colorectal cancer: mechanisms and precision interventions.Frontiers in oncology · 2026Review
- Gut microbiome-shaped chemotherapy responses across cancer types: mechanisms of resistance, biomarkers, and targeted interventions.Frontiers in immunology · 2026Review
- Gut microbial metabolites in cancer immunomodulation.Molecular cancer · 2025Review
- NOD2 reduces the chemoresistance of melanoma by inhibiting the TYMS/PLK1 signaling axis.Cell death & disease · 2024Article
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
The most commonly used chemotherapy for colorectal cancer (CRC) is the application of 5-fluorouracil (5-FU). Inhibition of thymidylate synthase (TYMS) expression appears to be a promising strategy to overcome the decreased sensitivity to 5-FU caused by high expression of TYMS, which can be induced by 5-FU treatment. Several compounds have been shown to potentially inhibit the expression of TYMS, but it is unclear whether short-chain fatty acids (SCFAs), which are naturally produced by bacteria in the human intestine, can regulate the expression of TYMS. Sodium butyrate (NaB) is the most widely known SCFA for its beneficial effects. Therefore, we investigated the enhancing effects on inhibition of cell viability and induction of apoptosis after co-treatment of NaB with 5-FU in two CRC cell lines, HCT116 and LoVo. This study suggests that the effect of NaB in improving therapeutic sensitivity to 5-FU in CRC cells may result from a mechanism that strongly inhibits the expression of TYMS. This study also shows that NaB inhibits the migration of CRC cells and can cause cell cycle arrest in the G2/M phase. These results suggest that NaB could be developed as a potential therapeutic adjuvant to improve the therapeutic effect of 5-FU in CRC.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.