ArticleCell & bioscience2024
NF-κB RelA is a cell-intrinsic metabolic checkpoint restricting glycolysis.
Article in Cell & bioscience, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 13 citations in OpenAlex.
- Exploring PDLIM2 as a prognostic biomarker and therapeutic target in lung adenocarcinoma.British journal of cancer · 2026Article
- Pentoxifylline targets TLR4/MyD88/NF-κB signaling to ameliorate neuroinflammation and metabolic dysfunction in a rat model of chronic hypoperfusion-induced vascular cognitive impairment.Metabolic brain disease · 2026Article
- An Advanced Single-Cell RNA Sequencing (scRNA-seq) Protocol Utilizing Custom-Designed Multiplexing.Bio-protocol · 2026Article
- PDLIM2 repression: a common mechanism in viral lung infection.ImmunoHorizons · 2026Article
- Emerging role of the immunoproteasome as a druggable target in lung inflammatory diseases.Respiratory research · 2026Review
- Bulk and Single-Cell Transcriptomics Reveal That SCO2 Drives Psoriasis via Activating CCR7International journal of molecular sciences · 2026Article
- A five-gene mitochondria-associated prognostic signature for bladder cancer.International journal of clinical and experimental pathology · 2026Article
- Macrophage metabolic reprogramming in organ transplantation: mechanisms, transplant outcomes, and therapeutic implications.Frontiers in cellular and infection microbiology · 2026Review
- Elucidating the therapeutic efficacy and mechanisms of arctigenin in ameliorating renal fibrosis: a combined transcriptomic and proteomic study.Frontiers in pharmacology · 2026Article
- PDLIM2 in Lung Adenocarcinoma Metastasis.bioRxiv : the preprint server for biology · 2025Article
- PDLIM2 Repression: A Common Mechanism in Viral Lung Infection.bioRxiv : the preprint server for biology · 2025Article
- NanoPDLIM2-Based Combination Therapy for Lung Cancer Treatment in Mouse Preclinical Studies.Bio-protocol · 2025Article
- Myeloid PDLIM2 repression as a common mechanism of infection susceptibility in lung diseases.Frontiers in immunology · 2025Article
- PDLIM2 is a novel E5 ubiquitin ligase enhancer that stabilizes ROC1 and recruits the ROC1-SCF ubiquitin ligase to ubiquitinate and degrade NF-κB RelA.Cell & bioscience · 2024Article
- NF-κB1 deficiency promotes macrophage-derived adrenal tumors but decreases neurofibromas in HTLV-I LTR-Tax transgenic mice.PloS one · 2024Article
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
Abstract
An intrinsic link between metabolism and function in immune cells, and in particular macrophages, has been well established recently. However, the molecular mechanisms controlling the metabolic switch in these sentinel cells for their integral roles in host defense, inflammation, homeostasis, and pathogenesis remain largely unknown. Here, we identify the master transcription factor NF-κB RelA as a vital cell-intrinsic checkpoint restricting aerobic glycolysis to favor mitochondrial oxidative phosphorylation (OXPHOS) and "M2" activation (alternative anti-inflammatory and pro-tumorigenic activation, in contrast to classical pro-inflammatory and anti-tumor M1 activation) of macrophages under oncogenic stress. RelA specific knockdown or genetic deletion in macrophages causes metabolism to shift away from OXPHOS toward glycolysis, resulting in drastically decreased oxygen consumption but significantly increased lactate and ATP production. The metabolic change in RelA deficient cells is associated with the decrease in the expressions of the OXPHOS gene SCO2 as well as the M2 marker and function genes arginase-1 and VEGF. These data suggest that RelA induces SCO2 expression to enhance OXPHOS and restrict glycolysis in macrophages for their pro-tumorigenic activation.
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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.