ArticleBMC cancer2010
Hypoxia induces differential translation of enolase/MBP-1.
Article in BMC cancer, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 49 papers.
What it found
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Who cites it
49 citing papers in PubMed, 88 citations in OpenAlex.
- c-Medical sciences (Basel, Switzerland) · 2026Review
- Enolase 1: A paradigm of metabolic enzyme moonlighting in tumorigenesis (Review).International journal of oncology · 2026Review
- Targeting Kupffer Cell Enolase 1 Attenuates Liver Inflammation and Injury in Hemorrhagic Shock.International journal of molecular sciences · 2025Article
- Hypoxia Induces Extensive Protein and Proteolytic Remodeling of the Cell Surface in Pancreatic Adenocarcinoma (PDAC) Cell Lines.Journal of proteome research · 2025Article
- The allergenic potential of enolases: physiological and pathophysiological insights.Current opinion in allergy and clinical immunology · 2025Review
- The role and therapeutic potential of glucose metabolism in multidrug resistance of cancer.Frontiers in cell and developmental biology · 2025Review
- Heterogeneous DNA methylation and gene expression patterns underly metabolic plasticity in canine astrocytoma-derived stem-like cells.Frontiers in oncology · 2025Article
- Article
- Tumour-specific phosphorylation of serine 419 drives alpha-enolase (ENO1) nuclear export in triple negative breast cancer progression.Cell & bioscience · 2024Article
- Glycolytic enzymes in non-glycolytic web: functional analysis of the key players.Cell biochemistry and biophysics · 2024Review
- Multifunctional roles of γ-enolase in the central nervous system: more than a neuronal marker.Cell & bioscience · 2024Review
- DeSUMOylation of a Verticillium dahliae enolase facilitates virulence by derepressing the expression of the effector VdSCP8.Nature communications · 2023Article
- c-MYC mediates the crosstalk between breast cancer cells and tumor microenvironment.Cell communication and signaling : CCS · 2023Review
- Review
- Lactate promotes the growth of patient-derived organoids from hepatopancreatobiliary cancers via ENO1/HIF1α pathway and does not affect their drug sensitivities.Cell death discovery · 2022Article
- ENO1 and Cancer.Molecular therapy oncolytics · 2022Review
- Integrated Metabolomics and Transcriptomic Analysis of Hepatopancreas in Different Living StatusAntioxidants (Basel, Switzerland) · 2021Article
- Implications of enolase in the RANKL-mediated osteoclast activity following spinal cord injury.Biocell : official journal of the Sociedades Latinoamericanas de Microscopia Electronica ... et. al · 2021Article
- More Than Meets the Eye Regarding Cancer Metabolism.International journal of molecular sciences · 2021Review
- Enolase 1, a Moonlighting Protein, as a Potential Target for Cancer Treatment.International journal of biological sciences · 2021Review
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundHypoxic microenvironments in tumors contribute to transformation, which may alter metabolism, growth, and therapeutic responsiveness. The alpha-enolase gene encodes both a glycolytic enzyme (alpha-enolase) and a DNA-binding tumor suppressor protein, c-myc binding protein (MBP-1). These divergent alpha-enolase gene products play central roles in glucose metabolism and growth regulation and their differential regulation may be critical for tumor adaptation to hypoxia. We have previously shown that MBP-1 and its binding to the c-myc P2 promoter regulates the metabolic and cellular growth changes that occur in response to altered exogenous glucose concentrations.
resultsTo examine the regulation of alpha-enolase and MBP-1 by a hypoxic microenvironment in breast cancer, MCF-7 cells were grown in low, physiologic, or high glucose under 1% oxygen. Our results demonstrate that adaptation to hypoxia involves attenuation of MBP-1 translation and loss of MBP-1-mediated regulation of c-myc transcription, evidenced by decreased MBP-1 binding to the c-myc P2 promoter. This allows for a robust increase in c-myc expression, "early c-myc response", which stimulates aerobic glycolysis resulting in tumor acclimation to oxidative stress. Increased alpha-enolase mRNA and preferential translation/post-translational modification may also allow for acclimatization to low oxygen, particularly under low glucose concentrations.
conclusionsThese results demonstrate that malignant cells adapt to hypoxia by modulating alpha-enolase/MBP-1 levels and suggest a mechanism for tumor cell induction of the hyperglycolytic state. This important "feedback" mechanism may help transformed cells to escape the apoptotic cascade, allowing for survival during limited glucose and oxygen availability.
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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.