ArticleJournal of experimental & clinical cancer research : CR2023
Mediation of PKM2-dependent glycolytic and non-glycolytic pathways by ENO2 in head and neck cancer development.
Article in Journal of experimental & clinical cancer research : CR, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.
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Who cites it
37 citing papers in PubMed, 55 citations in OpenAlex.
- ENO1 promotes acute myeloid leukemia progression through SCD1-mediated lipid metabolism reprogramming.Blood advances · 2026Article
- ENO2 sustains cancer stemness and metastatic competence through a phosphoenolpyruvate-dependent metabolic axis in triple-negative breast cancer.Cell death & disease · 2026Article
- GLS1 Orchestrates Exosome-Mediated Tumor-Endothelial Communication to Facilitate Angiogenesis.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Review
- Enolase 2-mediated lactylation-dependent disruption of the GNL3-MDM2-p53 axis in age-related osteoarthritis.Cellular & molecular biology letters · 2026Article
- Lipid Metabolic Rewiring During Continuous Prostate Cancer Progression Defines a Biologically Relevant Four-Gene Prognostic Signature.Biological procedures online · 2026Article
- H4K5 lactylation - ENO2 loop drives glycolysis and HCC progression.JHEP reports : innovation in hepatology · 2026Article
- Comprehensive analysis and validation of the prognostic value of glycosylation- and mitophagy-related genes for head and neck squamous cell carcinoma.Translational cancer research · 2026Article
- [Research progress on the metabolic regulatory mechanisms of coronary collateral circulation].Zhong nan da xue xue bao. Yi xue ban = Journal of Central South University. Medical sciences · 2026Review
- Cancer metabolism: bridging tumorigenesis mechanisms to treatment susceptibility.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2026Review
- M2 macrophages promote lymphatic metastasis by regulating PKM2 nuclear translocation in triple-negative breast cancer.Cell death & disease · 2026Article
- Targeting Glycolytic Metabolism in Cancer Therapy: Current Approaches and Future Perspectives.Cells · 2026Review
- Processes and therapeutic perspectives of acylation modifications of lysine and cysteine in tumors.Cell communication and signaling : CCS · 2026Review
- The deubiquitinating enzyme UCHL3 promotes bladder cancer progression and glycolysis through enhancing PKM2 protein stability.Frontiers in oncology · 2026Article
- Metabolic cell deaths in head and neck cancer: mechanisms, therapeutic potential, and challenges.Annals of medicine · 2025Review
- Metabolomic and transcriptomic profiling of HNSCC identifies AMIGO2 as a therapeutic target modulating tumor microenvironment.NPJ precision oncology · 2025Article
- ENO2 regulates CD4mBio · 2025Article
- Expanding the Knowledge of the Molecular Effects and Therapeutic Potential of Incomptine A for the Treatment of Non-Hodgkin Lymphoma: In Vivo and Bioinformatics Studies, Part III.Pharmaceuticals (Basel, Switzerland) · 2025Article
- Molecular signatures of disulfidptosis: interplay with programmed cell death pathways and therapeutic implications in oncology.Cellular & molecular biology letters · 2025Review
- Exploring glycolytic enzymes in disease: potential biomarkers and therapeutic targets in neurodegeneration, cancer and parasitic infections.Open biology · 2025Review
Corrections and comments
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Authors and funding
9 authors at 3 institutions in 2 countries.
Funding
Abstract
backgroundEnolase 2 (ENO2) is a crucial glycolytic enzyme in cancer metabolic process and acts as a "moonlighting" protein to play various functions in diverse cellular processes unrelated to glycolysis. ENO2 is highly expressed in head and neck squamous cell carcinoma (HNSCC) tissues relative to normal tissues; however, its impact and underlying regulatory mechanisms in HNSCC malignancy remain unclear.
methodsMolecular alterations were examined by bioinformatics, qRT-PCR, western blotting, immunofluorescence, immunohistochemistry, immunoprecipitation, and ChIP-PCR assays. Metabolic changes were assessed by intracellular levels of ATP and glucose. Animal study was used to evaluate the therapeutic efficacy of the ENO inhibitor.
resultsENO2 is required for HNSCC cell proliferation and glycolysis, which, surprisingly, is partially achieved by controlling PKM2 protein stability and its nuclear translocation. Mechanistically, loss of ENO2 expression promotes PKM2 protein degradation via the ubiquitin-proteasome pathway and prevents the switch of cytoplasmic PKM2 to the nucleus by inactivating AKT signaling, leading to a blockade in PKM2-mediated glycolytic flux and CCND1-associated cell cycle progression. In addition, treatment with the ENO inhibitor AP-III-a4 significantly induces HNSCC remission in a preclinical mouse model.
conclusionOur work elucidates the signaling basis underlying ENO2-dependent HNSCC development, providing evidence to establish a novel ENO2-targeted therapy for treating HNSCC.
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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.