ArticleMolecular metabolism2023
C/EBPβ-LIP mediated activation of the malate-aspartate shuttle sensitizes cells to glycolysis inhibition.
Article in Molecular metabolism, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
What it found
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Who cites it
6 citing papers in PubMed, 10 citations in OpenAlex.
- The transcription factor C/EBPβ promotes hyperglycemia-elicited glycolysis and liver cancer progression.Nature communications · 2026Article
- Why is the tumor microenvironment disordered by NADH/NADRedox biology · 2026Review
- Enhanced C/EBPα Function Extends Healthspan and Lifespan in the African Turquoise Killifish.Aging cell · 2025Article
- Organoid models of ovarian cancer: resolving immune mechanisms of metabolic reprogramming and drug resistance.Frontiers in immunology · 2025Review
- Proteomic and metabolomic insights into oxidative stress response activation in mouse embryos generated byHuman reproduction open · 2025Article
- AI-assisted mass spectrometry imaging withChemical science · 2024Article
Corrections and comments
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Authors and funding
9 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
objectiveCancer cells use glycolysis for generation of metabolic intermediates and ATP needed for cell growth and proliferation. The transcription factor C/EBPβ-LIP stimulates glycolysis and mitochondrial respiration in cancer cells. We initially observed that high expression of C/EBPβ-LIP makes cells vulnerable to treatment with the glycolysis inhibitor 2-deoxyglucose. The aim of the study was to uncover the involved mechanisms of C/EBPβ-LIP induced sensitivity to glycolysis inhibition.
methodsWe used genetically engineered cell lines to examine the effect of C/EBPβ-LIP and -LAP protein isoforms on glycolysis and NADH/NAD
resultsThe transcription factor C/EBPβ-LIP stimulates both glycolysis and the malate-aspartate shuttle (MAS) and increases the sensitivity to glycolysis inhibition (2-deoxyglucose) in fibroblasts and breast cancer cells. Inhibition of glycolysis with ongoing C/EBPβ-LIP-induced MAS activity results in NADH depletion and apoptosis that can be rescued by inhibiting either the MAS or other NAD
conclusionThis study indicates that a low NADH/NAD+ ratio is an essential mediator of 2-deoxyglucose toxicity in cells with high cytoplasmic NAD
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