ArticleCell death & disease2026
Targeting ENO1 reprograms macrophage polarization to trigger antitumor immunity and improves the therapeutic effect of radiotherapy.
Article in Cell death & disease, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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The trial behind it
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Who cites it
4 citing papers in PubMed.
- ENO1 as an Immunoregulatory Hub in Cancer: Mechanisms and Translational Implications.Biomolecules · 2026Review
- ENO1 as a Central Regulator Linking Metabolic Reprogramming to Tumor Plasticity.International journal of molecular sciences · 2026Review
- Breast Cancer Milieu Maneuvers Cancer-Associated Macrophages to Synergize Neoplastic Repertoires.Cancers · 2026Review
- GUDCA drives colorectal cancer progression via ALKBH5-mediated m6A modification of ENO1 and glycolytic reprogramming.Frontiers in pharmacology · 2026Article
Corrections and comments
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Authors and funding
13 authors.
Funding
Abstract
Enolase 1 (ENO1) is a glycolytic enzyme involved in tumor progression that performs a variety of classical and nonclassical functions. However, the mechanism by which it promotes tumor progression is still not fully understood. Here, we revealed that TGFβ1/Smad3 signaling triggered the symmetric dimethylation of arginine (SDMA) on ENO1 by protein arginine methyltransferase 5 (PRMT5), leading to membranous ENO1 translocation. Surface ENO1 interacts with monocarboxylate transporter 4 (MCT4) for lactate secretion, which recruits M2 macrophages and promotes an immunosuppressive tumor microenvironment (TME). Targeting surface ENO1 with HuL001, a first-in-class humanized antibody, significantly reduced glycolysis, decreased extracellular lactate accumulation, reprogrammed macrophage polarization and inhibited tumor growth and distant metastasis. Moreover, targeting surface ENO1 significantly increased the therapeutic response to radiotherapy and delayed tumor regrowth by increasing antitumoral M1 macrophages and cytotoxic CD8
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Registered trials
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