ReviewFrontiers in oncology2017
Metabolic Plasiticy in Cancers-Distinct Role of Glycolytic Enzymes GPI, LDHs or Membrane Transporters MCTs.
Review in Frontiers in oncology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
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Who cites it
29 citing papers in PubMed, 47 citations in OpenAlex.
- Lactate as a Signaling Molecule in the Tumor Microenvironment: Implications for Cancer Progression.Biochemical genetics · 2026Review
- Flipping the Target: Evaluating Natural LDHA Inhibitors for Selective LDHB Modulation.Molecules (Basel, Switzerland) · 2025Article
- Glucose metabolism transcriptome clustering identifies subsets of resectable lung adenocarcinoma with different prognoses.JTCVS open · 2024Article
- Metabolic priming by multiple enzyme systems supports glycolysis, HIF1α stabilisation, and human cancer cell survival in early hypoxia.The EMBO journal · 2024Article
- Exosome proteomes reveal glycolysis-related enzyme enrichment in primary canine mammary gland tumor compared to metastases.Proteome science · 2024Article
- Systematic analysis of the role of LDHs subtype in pan-cancer demonstrates the importance of LDHD in the prognosis of hepatocellular carcinoma patients.BMC cancer · 2024Article
- Metabolic Phenotype Intricacies on Altered Glucose Metabolism of Breast Cancer Cells upon Glut-1 Inhibition and Mimic Hypoxia In Vitro.Applied biochemistry and biotechnology · 2023Article
- LncRNA RP11-620J15.3 promotes HCC cell proliferation and metastasis by targeting miR-326/GPI to enhance glycolysis.Biology direct · 2023Article
- Metabolic Rewiring toward Oxidative Phosphorylation Disrupts Intrinsic Resistance to Ferroptosis of the Colon Adenocarcinoma Cells.Antioxidants (Basel, Switzerland) · 2022Article
- Identification of metabolic pathways underlying FGF1 and CHIR99021-mediated cardioprotection.iScience · 2022Article
- Oncogene-mediated metabolic gene signature predicts breast cancer outcome.NPJ breast cancer · 2021Article
- Metabolic Strategies for Inhibiting Cancer Development.Advances in nutrition (Bethesda, Md.) · 2021Review
- Metabolic Profile in Neonatal Pig Hearts.Frontiers in cardiovascular medicine · 2021Article
- Circular RNAs Regulate Glucose Metabolism in Cancer Cells.OncoTargets and therapy · 2021Review
- Glucose Concentration in Cell Culture Medium Influences the BRCA1-Mediated Regulation of the Lipogenic Action of IGF-I in Breast Cancer Cells.International journal of molecular sciences · 2020Article
- Lactate in the Tumor Microenvironment: An Essential Molecule in Cancer Progression and Treatment.Cancers · 2020Review
- Energy metabolism in cancer stem cells.World journal of stem cells · 2020Review
- Warburg and Beyond: The Power of Mitochondrial Metabolism to Collaborate or Replace Fermentative Glycolysis in Cancer.Cancers · 2020Review
- Article
- Lactate-Protected Hypoglycemia (LPH).Frontiers in neuroscience · 2020Article
Corrections and comments
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Authors and funding
5 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Research on cancer metabolism has recently re-surfaced as a major focal point in cancer field with a reprogrammed metabolism no longer being considered as a mere consequence of oncogenic transformation, but as a hallmark of cancer. Reprogramming metabolic pathways and nutrient sensing is an elaborate way by which cancer cells respond to high bioenergetic and anabolic demands during tumorigenesis. Thus, inhibiting specific metabolic pathways at defined steps should provide potent ways of arresting tumor growth. However, both animal models and clinical observations have revealed that this approach is seriously limited by an extraordinary cellular metabolic plasticity. The classical example of cancer metabolic reprogramming is the preference for aerobic glycolysis, or Warburg effect, where cancers increase their glycolytic flux and produce lactate regardless of the presence of the oxygen. This allows cancer cells to meet the metabolic requirements for high rates of proliferation. Here, we discuss the benefits and limitations of disrupting fermentative glycolysis for impeding tumor growth at three levels of the pathway: (i) an upstream block at the level of the glucose-6-phosphate isomerase (GPI), (ii) a downstream block at the level of lactate dehydrogenases (LDH, isoforms A and B), and (iii) the endpoint block preventing lactic acid export (MCT1/4). Using these examples of genetic disruption targeting glycolysis studied in our lab, we will discuss the responses of different cancer cell lines in terms of metabolic rewiring, growth arrest, and tumor escape and compare it with the broader literature.
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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.