ArticleOncotarget2016
Hypoxia-mediated upregulation of MCT1 expression supports the glycolytic phenotype of glioblastomas.
Article in Oncotarget, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 65 papers, 1 of them a synthesis that pooled it.
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Who cites it
65 citing papers in PubMed, 1 synthesis or guideline pooled it, 129 citations in OpenAlex.
- Hydrated proton complexes supplementation for tumor microenvironment reprogramming: a bioenergetic strategy targeting the Warburg effect and mitochondrial dysfunction.Frontiers in oncology · 2025Pooled it
- Review
- Redox Homeostasis, Metabolic Pathways and Plasticity in Uveal Melanoma Compared to Other Cancers.Cancers · 2026Review
- MCT4 mediates hypoxia-induced extracellular lactate release from IPF fibroblasts.American journal of respiratory cell and molecular biology · 2026Article
- MCT1 as a critical regulator of insulin signaling, energy homeostasis and podocyte function.Scientific reports · 2026Article
- Lactate-Mediated Epigenetic and Immunometabolic Reprogramming in Glioma: An Emerging Axis Linking Metabolism to Tumor Progression.Biomedicines · 2025Review
- Restricting metabolic plasticity enhances stress adaptation through the modulation of PDH and HIF1A in TRAP1-depleted colon cancer.Cancer letters · 2025Article
- Utilizing Monocarboxylate Transporter 1-Mediated Blood-Brain Barrier Penetration for Glioblastoma Positron Emission Tomography Imaging with 6-[Molecular pharmaceutics · 2025Article
- Immune response recalibration using immune therapy and biomimetic nano-therapy against high-grade gliomas and brain metastases.Asian journal of pharmaceutical sciences · 2025Review
- Lactate metabolism and histone lactylation in the central nervous system disorders: impacts and molecular mechanisms.Journal of neuroinflammation · 2024Review
- Tumor hypoxia unveiled: insights into microenvironment, detection tools and emerging therapies.Clinical and experimental medicine · 2024Review
- Hypoxia-mediated repression of pyruvate carboxylase drives immunosuppression.Breast cancer research : BCR · 2024Article
- Preconditioning-Induced Facilitation of Lactate Release from Astrocytes Is Essential for Brain Ischemic Tolerance.eNeuro · 2024Article
- Evolutionary dynamics of glucose-deprived cancer cells: insights from experimentally informed mathematical modelling.Journal of the Royal Society, Interface · 2024Article
- 2P-FLIM unveils time-dependent metabolic shifts during osteogenic differentiation with a key role of lactate to fuel osteogenesis via glutaminolysis identified.Stem cell research & therapy · 2023Article
- Targeting Glucose Metabolism in Cancer Cells as an Approach to Overcoming Drug Resistance.Pharmaceutics · 2023Review
- Metabolic Profiles Point Out Metabolic Pathways Pivotal in Two Glioblastoma (GBM) Cell Lines, U251 and U-87MG.Biomedicines · 2023Article
- The role of noncoding RNAs in metabolic reprogramming of cancer cells.Cellular & molecular biology letters · 2023Review
- The Oxygen Cascade from Atmosphere to Mitochondria as a Tool to Understand the (Mal)adaptation to Hypoxia.International journal of molecular sciences · 2023Review
- Recent advances in label-free optical, electrochemical, and electronic biosensors for glioma biomarkers.Biomicrofluidics · 2023Review
5 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
13 authors at 5 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundGlioblastomas (GBM) present a high cellular heterogeneity with conspicuous necrotic regions associated with hypoxia, which is related to tumor aggressiveness. GBM tumors exhibit high glycolytic metabolism with increased lactate production that is extruded to the tumor microenvironment through monocarboxylate transporters (MCTs). While hypoxia-mediated regulation of MCT4 has been characterized, the role of MCT1 is still controversial. Thus, we aimed to understand the role of hypoxia in the regulation of MCT expression and function in GBM, MCT1 in particular.
methodsExpression of hypoxia- and glycolytic-related markers, as well as MCT1 and MCT4 isoforms was assessed in in vitro and in vivo orthotopic glioma models, and also in human GBM tissues by immunofluorescence/immunohistochemistry and Western blot. Following MCT1 inhibition, either pharmacologically with CHC (α-cyano-4-hydroxynnamic acid) or genetically with siRNAs, we assessed GBM cell viability, proliferation, metabolism, migration and invasion, under normoxia and hypoxia conditions.
resultsHypoxia induced an increase in MCT1 plasma membrane expression in glioma cells, both in in vitro and in vivo models. Additionally, treatment with CHC and downregulation of MCT1 in glioma cells decreased lactate production, cell proliferation and invasion under hypoxia. Moreover, in the in vivo orthotopic model and in human GBM tissues, there was extensive co-expression of MCT1, but not MCT4, with the GBM hypoxia marker CAIX.
conclusionHypoxia-induced MCT1 supports GBM glycolytic phenotype, being responsible for lactate efflux and an important mediator of cell survival and aggressiveness. Therefore, MCT1 constitutes a promising therapeutic target in GBM.
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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.