ArticleThe EMBO journal2024
PKM2 functions as a histidine kinase to phosphorylate PGAM1 and increase glycolysis shunts in cancer.
Article in The EMBO journal, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
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Who cites it
27 citing papers in PubMed.
- Review
- Targeting PGAM1 Y119 phosphorylation resensitizes non-small-cell lung cancer to cisplatin therapy by promoting oxidative stress and DNA damage.The Journal of biological chemistry · 2026Article
- PGAM1 rheostat in glycolysis and autophagy.Nature cell biology · 2026Article
- Post-translational modifications in metabolic reprogramming: implications for metabolic therapy and immunotherapy in cancer.Signal transduction and targeted therapy · 2026Review
- USP20-mediated PGAM1 stabilization promotes glycolysis and confers osimertinib resistance in non-small cell lung carcinoma.Oncogene · 2026Article
- The evolving landscape of the Warburg effect in gastric cancer: From molecular mechanisms to targeted therapy.Clinical and translational medicine · 2026Review
- The regulatory role of circGDI2 in hepatocellular carcinoma proliferation and glycolysis with the involvement of m6A modification.Non-coding RNA research · 2026Article
- Targeting Glycolytic Metabolism in Cancer Therapy: Current Approaches and Future Perspectives.Cells · 2026Review
- REEP6 promotes colorectal cancer glycolysis and tumorigenesis through PRMT5-mediated PGAM1 arginine methylation.Acta pharmaceutica Sinica. B · 2026Article
- A Cori cycle-related gene signature predicts prognosis, immune microenvironment, and drug response in breast cancer.Translational cancer research · 2026Article
- GUDCA drives colorectal cancer progression via ALKBH5-mediated m6A modification of ENO1 and glycolytic reprogramming.Frontiers in pharmacology · 2026Article
- High Glycolysis and Lipid Metabolism Status Predicts Poor Prognosis in Colorectal Cancer Patients.Current molecular medicine · 2026Article
- O- and N-Phosphoproteomic Analysis Using Online Alkaline-pH Reversed-Phase Nanoelectrospray-Tandem Mass Spectrometry.Methods in molecular biology (Clifton, N.J.) · 2026Article
- ILKAP drives hepatocellular carcinoma progression by modulating PGAM1-mediated glycolytic reprogramming.Frontiers of medicine · 2025Article
- Review
- Conformational Dynamics of PKM2 Regulate Hypoxia-Induced Pathological Retinal Angiogenesis.Investigative ophthalmology & visual science · 2025Article
- Serum p-Cresol and 7-HOCA Levels and Fatty Acid and Purine Metabolism Are Associated with Survival, Progression, and Molecular Classification in GB-Serum Proteome and Metabolome Analysis Pre vs. Post Up-Front Chemoirradiation.Current oncology (Toronto, Ont.) · 2025Article
- Lactylation-induced ALKBH5 targets RNF123 to worsen retinal Müller cell activation through PKM2-regulated Glycolysis in diabetic retinopathy.Journal of translational medicine · 2025Article
- Transcriptomic analysis identifies key genes associated with nutrient deprivation responses in infectious bursal disease virus infection.BMC genomics · 2025Article
- Dihydrotanshinone I Targets PGAM1 to Induce SYVN1-Mediated Ubiquitination and Suppress Glycolysis in Hepatocellular Carcinoma.Phytotherapy research : PTR · 2025Article
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Authors and funding
19 authors.
Funding
Abstract
Phosphoglycerate mutase 1 (PGAM1) is a key node enzyme that diverts the metabolic reactions from glycolysis into its shunts to support macromolecule biosynthesis for rapid and sustainable cell proliferation. It is prevalent that PGAM1 activity is upregulated in various tumors; however, the underlying mechanism remains unclear. Here, we unveil that pyruvate kinase M2 (PKM2) moonlights as a histidine kinase in a phosphoenolpyruvate (PEP)-dependent manner to catalyze PGAM1 H11 phosphorylation, that is essential for PGAM1 activity. Moreover, monomeric and dimeric but not tetrameric PKM2 are efficient to phosphorylate and activate PGAM1. In response to epidermal growth factor signaling, Src-catalyzed PGAM1 Y119 phosphorylation is a prerequisite for PKM2 binding and the subsequent PGAM1 H11 phosphorylation, which constitutes a discrepancy between tumor and normal cells. A PGAM1-derived pY119-containing cell-permeable peptide or Y119 mutation disrupts the interaction of PGAM1 with PKM2 and PGAM1 H11 phosphorylation, dampening the glycolysis shunts and tumor growth. Together, these results identify a function of PKM2 as a histidine kinase, and illustrate the importance of enzyme crosstalk as a regulatory mode during metabolic reprogramming and tumorigenesis.
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