ArticleNature cell biology2015
AMPK and PFKFB3 mediate glycolysis and survival in response to mitophagy during mitotic arrest.
Article in Nature cell biology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 161 papers, 1 of them a synthesis that pooled it.
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The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
161 citing papers in PubMed, 1 synthesis or guideline pooled it, 267 citations in OpenAlex.
- Prognostic Significance of the Metabolic Marker Hexokinase-2 in Various Solid Tumors: A Meta-Analysis.PloS one · 2016Pooled it
- Biomarker analysis of the MITO2 phase III trial of first-line treatment in ovarian cancer: predictive value of DNA-PK and phosphorylated ACC.Oncotarget · 2016Trial
- Metabolic links between mitochondrial electron transport, glycolysis, and AMP-activated protein kinase signaling modulate hepatocellular carcinoma cell survival.Molecular and cellular biochemistry · 2026Article
- The dual role of AMPK in cancer metabolic reprogramming.Molecular biology reports · 2026Review
- Integrated Physiological and Transcriptomic Analyses Suggest Key Adaptive Mechanisms of European Perch (Animals : an open access journal from MDPI · 2026Article
- (+)-Miliusol suppresses the Warburg effect and induces regulated cell death in triple-negative breast cancer through targeting EIF3D and remodeling cancer metabolism.Acta pharmaceutica Sinica. B · 2026Article
- Proteomic Identification of PFKFB3 and PFKFB4 Associated with Coenzyme Metabolism and Redox Imbalance in Dairy Cows with Clinical Mastitis.Antioxidants (Basel, Switzerland) · 2026Article
- The moonlighting functions of glycolytic enzymes in tumorigenesis.Cellular oncology (Dordrecht, Netherlands) · 2026Review
- Tumor-associated macrophages promote chemoresistance to Paclitaxel via activating NOTCH2-JAG1 juxtacrine signaling.Molecular cancer · 2026Article
- Mechanical forces orchestrate the epigenetic landscape of oral mesenchymal stem/progenitor cell fate in dental and periodontal tissues.Frontiers in cell and developmental biology · 2026Review
- Targeting phosphofructokinase in cancer: integrating natural products for metabolic reprogramming and therapeutic innovation.Frontiers in pharmacology · 2026Review
- Cold atmospheric plasma is a promising strategy for treating diabetic retinopathy.Journal of translational medicine · 2025Review
- Pregnane X receptor (PXR) as a prognostic marker and therapeutic target in kidney renal clear cell carcinoma (KIRC) via AMPK pathway regulation.Scientific reports · 2025Article
- Mitochondrial Quality Control in Health and Disease.MedComm · 2025Review
- PFKFB3-Mediated Glycolytic Metabolic Reprogramming Regulates Inflammatory Response in Dry Eye Disease.Investigative ophthalmology & visual science · 2025Article
- A Newly Identified Protective Role of C5a Receptor 1 in Kidney Tubules against Toxin-Induced Acute Kidney Injury.The American journal of pathology · 2025Article
- PFKFB3 ameliorates ischemia-induced neuronal damage by reducing reactive oxygen species and inhibiting nuclear translocation of Cdk5.Scientific reports · 2024Article
- Therapeutic modulation of ROCK overcomes metabolic adaptation of cancer cells to OXPHOS inhibition and drives synergistic anti-tumor activity.bioRxiv : the preprint server for biology · 2024Article
- Acetylation of PGK1 at lysine 323 promotes glycolysis, cell proliferation, and metastasis in luminal A breast cancer cells.BMC cancer · 2024Article
- AMPK drives both glycolytic and oxidative metabolism in murine and human T cells during graft-versus-host disease.Blood advances · 2024Article
101 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
19 authors at 7 institutions in 2 countries.
Funding
Abstract
Blocking mitotic progression has been proposed as an attractive therapeutic strategy to impair proliferation of tumour cells. However, how cells survive during prolonged mitotic arrest is not well understood. We show here that survival during mitotic arrest is affected by the special energetic requirements of mitotic cells. Prolonged mitotic arrest results in mitophagy-dependent loss of mitochondria, accompanied by reduced ATP levels and the activation of AMPK. Oxidative respiration is replaced by glycolysis owing to AMPK-dependent phosphorylation of PFKFB3 and increased production of this protein as a consequence of mitotic-specific translational activation of its mRNA. Induction of autophagy or inhibition of AMPK or PFKFB3 results in enhanced cell death in mitosis and improves the anti-tumoral efficiency of microtubule poisons in breast cancer cells. Thus, survival of mitotic-arrested cells is limited by their metabolic requirements, a feature with potential implications in cancer therapies aimed to impair mitosis or metabolism in tumour cells.
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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.