ArticleScientific reports2022
Pyruvate kinase M1 regulates butyrate metabolism in cancerous colonocytes.
Article in Scientific reports, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 20 citations in OpenAlex.
- Review
- Butyric glycerides enhance resistance of chicken enterocytes to pathogen adhesion and cytotoxicity in vitro.Veterinary research communications · 2026Article
- PKM2 is a key regulator of cardiac lipid metabolism in mice.Mitochondrion · 2025Article
- Elucidating the Role and Mechanism of Alpha-Enolase in Senescent Amelioration via Metabolic Reprogramming.Cell proliferation · 2025Article
- MicroRNAs and their role in breast cancer metabolism (Review).International journal of oncology · 2025Review
- HDAC inhibitor MS275 reprograms metabolism to induce differentiation and suppress proliferation in hepatocellular carcinoma.Frontiers in immunology · 2025Article
- Role of glucose metabolic reprogramming in colorectal cancer progression and drug resistance.Translational oncology · 2024Review
- Fecal Microbiota Transplantation: Insights into Colon Carcinogenesis and Immune Regulation.Journal of clinical medicine · 2024Review
- Gut microbiota-derived short-chain fatty acids regulate gastrointestinal tumor immunity: a novel therapeutic strategy?Frontiers in immunology · 2023Review
- Targeted splicing therapy: new strategies for colorectal cancer.Frontiers in oncology · 2023Review
- Proteome profiling of endogenous and potential S-nitrosylation in colorectal cancer.Frontiers in endocrinology · 2023Article
- Review
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
Abstract
Colorectal cancer (CRC) cells shift metabolism toward aerobic glycolysis and away from using oxidative substrates such as butyrate. Pyruvate kinase M1/2 (PKM) is an enzyme that catalyzes the last step in glycolysis, which converts phosphoenolpyruvate to pyruvate. M1 and M2 are alternatively spliced isoforms of the Pkm gene. The PKM1 isoform promotes oxidative metabolism, whereas PKM2 enhances aerobic glycolysis. We hypothesize that the PKM isoforms are involved in the shift away from butyrate oxidation towards glycolysis in CRC cells. Here, we find that PKM2 is increased and PKM1 is decreased in human colorectal carcinomas as compared to non-cancerous tissue. To test whether PKM1/2 alter colonocyte metabolism, we created a knockdown of PKM2 and PKM1 in CRC cells to analyze how butyrate oxidation and glycolysis would be impacted. We report that butyrate oxidation in CRC cells is regulated by PKM1 levels, not PKM2. Decreased butyrate oxidation observed through knockdown of PKM1 and PKM2 is rescued through re-addition of PKM1. Diminished PKM1 lowered mitochondrial basal respiration and decreased mitochondrial spare capacity. We demonstrate that PKM1 suppresses glycolysis and inhibits hypoxia-inducible factor-1 alpha. These data suggest that reduced PKM1 is, in part, responsible for increased glycolysis and diminished butyrate oxidation in CRC cells.
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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 Socratic graph.