ArticleNature cell biology2011
NF-κB controls energy homeostasis and metabolic adaptation by upregulating mitochondrial respiration.
Article in Nature cell biology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 228 papers.
What it found
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Who cites it
228 citing papers in PubMed, 399 citations in OpenAlex.
- Acute exercise leads to regulation of telomere-associated genes and microRNA expression in immune cells.PloS one · 2014Trial
- Metabolic reprogramming in colorectal cancer: Mechanisms and therapeutic insights.Genes & diseases · 2027Review
- The NF-κB Isoform p65 iso5 Is Associated with Distinct Transcriptional Programs and Signaling Pathways.Cells · 2026Article
- TKTL1 mediates metabolic adaptation and stress resistance in pancreatic cancer cells under nutrient-deprived conditions.Oncogene · 2026Article
- Carboxylesterase 1 is a core metabolic vulnerability of platinum-resistant high-grade serous ovarian carcinoma.Journal of experimental & clinical cancer research : CR · 2026Article
- The alternative NF-κB RelB subunit is a novel critical sensor of lipid metabolism to promote tumor development.Cell death & disease · 2026Article
- Spatiotemporal control of mitoribosome-mediated metabolic reprogramming in cancer: implications for heterogeneity and therapeutic targeting.Frontiers in cell and developmental biology · 2026Review
- Cell-Free DNA (cfDNA), Its Applications in Cancer Diagnosis and Monitoring, and Its Potential Role in Regulating Cancer Metabolism.Advances in experimental medicine and biology · 2026Review
- Pioglitazone Modulates p65-Mediated Mitochondrial Bioenergetics: Implications for Acetaldehyde-Induced HIV Replication in Alveolar Macrophages.Biomolecules · 2025Article
- Natural products as therapeutic interventions for inflammation-mediated cancer.Discover oncology · 2025Review
- Mitochondrial complex III-derived ROS amplify immunometabolic changes in astrocytes and promote dementia pathology.Nature metabolism · 2025Article
- SUCNR1 Deficiency Alleviates Liver Ischemia-Reperfusion Injury by Regulating Kupffer Cell Activation and Polarization Through the ERK/NF-κB Pathway in Mice.Inflammation · 2025Article
- Balancing Decidualization, Autophagy, and Cellular Senescence for Reproductive Success in Endometriosis Biology.International journal of molecular sciences · 2025Review
- Macrophage-derived IL-1β directs fibroblast progenitor cell fate via metabolic reprogramming in wound healing.Communications biology · 2025Article
- NF-κB in inflammation and cancer.Cellular & molecular immunology · 2025Review
- NF-κB and apoptosis: colorectal cancer progression and novel strategies for treatment.European journal of medical research · 2025Review
- L2S2: chemical perturbation and CRISPR KO LINCS L1000 signature search engine.Nucleic acids research · 2025Article
- Metabolic hallmarks of trastuzumab resistance.Expert opinion on therapeutic targets · 2025Review
- The molecular mechanism of NF-κB dysregulation across different subtypes of renal cell carcinoma.Journal of advanced research · 2025Review
- NF-κB-mediated developmental delay extends lifespan inProceedings of the National Academy of Sciences of the United States of America · 2025Article
168 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
12 authors at 6 institutions in 3 countries.
Funding
Abstract
Cell proliferation is a metabolically demanding process. It requires active reprogramming of cellular bioenergetic pathways towards glucose metabolism to support anabolic growth. NF-κB/Rel transcription factors coordinate many of the signals that drive proliferation during immunity, inflammation and oncogenesis, but whether NF-κB regulates the metabolic reprogramming required for cell division during these processes is unknown. Here, we report that NF-κB organizes energy metabolism networks by controlling the balance between the utilization of glycolysis and mitochondrial respiration. NF-κB inhibition causes cellular reprogramming to aerobic glycolysis under basal conditions and induces necrosis on glucose starvation. The metabolic reorganization that results from NF-κB inhibition overcomes the requirement for tumour suppressor mutation in oncogenic transformation and impairs metabolic adaptation in cancer in vivo. This NF-κB-dependent metabolic pathway involves stimulation of oxidative phosphorylation through upregulation of mitochondrial synthesis of cytochrome c oxidase 2 (SCO2; ref. ). Our findings identify NF-κB as a physiological regulator of mitochondrial respiration and establish a role for NF-κB in metabolic adaptation in normal cells and cancer.
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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.