ArticleBiochimica et biophysica acta2015
AMPKα1 deficiency promotes cellular proliferation and DNA damage via p21 reduction in mouse embryonic fibroblasts.
Article in Biochimica et biophysica acta, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 22 citations in OpenAlex.
- Acute Cold Exposure Cell-Autonomously Reduces mTORC1 Signaling and Protein Synthesis Independent of AMPK.Cells · 2025Article
- DNA Damage and Nuclear Morphological Changes in Cardiac Hypertrophy Are Mediated by SNRK Through Actin Depolymerization.Circulation · 2023Article
- DNA damage and nuclear morphological changes in cardiac hypertrophy are mediated by SNRK through actin depolymerization.bioRxiv : the preprint server for biology · 2023Article
- Evolution of Natural Product Scaffolds as Potential Proteasome Inhibitors in Developing Cancer Therapeutics.Metabolites · 2023Review
- Phosphoproteomics Reveals the AMPK Substrate Network in Response to DNA Damage and Histone Acetylation.Genomics, proteomics & bioinformatics · 2022Article
- AMPKα1 deletion in myofibroblasts exacerbates post-myocardial infarction fibrosis by a connexin 43 mechanism.Basic research in cardiology · 2021Article
- Sirt-1 Regulates Physiological Process and Exerts Protective Effects against Oxidative Stress.BioMed research international · 2021Article
- Loss of AMPKalpha1 Triggers Centrosome Amplification via PLK4 Upregulation in Mouse Embryonic Fibroblasts.International journal of molecular sciences · 2020Article
- AMPK Activity Contributes to G2 Arrest and DNA Damage Decrease via p53/p21 Pathways in Oxidatively Damaged Mouse Zygotes.Frontiers in cell and developmental biology · 2020Article
- AMP-activated protein kinase α1 serves a carcinogenic role via regulation of vascular endothelial growth factor expression in patients with non-small cell lung cancer.Oncology letters · 2019Article
- β-Hydroxybutyrate Prevents Vascular Senescence through hnRNP A1-Mediated Upregulation of Oct4.Molecular cell · 2018Article
- Liver kinase B1/adenosine monophosphate-activated protein kinase signaling axis induces p21/WAF1 expression in a p53-dependent manner.Oncology letters · 2018Article
- Allyl Isothiocyanate Exhibits No Anticancer Activity in MDA-MB-231 Breast Cancer Cells.International journal of molecular sciences · 2018Article
- Energy sensing pathways: Bridging type 2 diabetes and colorectal cancer?Journal of diabetes and its complications · 2017Review
- AMPKα1 deletion in fibroblasts promotes tumorigenesis in athymic nude mice by p52-mediated elevation of erythropoietin and CDK2.Oncotarget · 2016Article
- HBP1-mediated Regulation of p21 Protein through the Mdm2/p53 and TCF4/EZH2 Pathways and Its Impact on Cell Senescence and Tumorigenesis.The Journal of biological chemistry · 2016Article
- Absence of AMPKα2 accelerates cellular senescence via p16 induction in mouse embryonic fibroblasts.The international journal of biochemistry & cell biology · 2016Article
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Authors and funding
8 authors at 2 institutions in 2 countries.
Funding
Abstract
Emerging evidence suggests that activation of adenosine monophosphate-activated protein kinase (AMPK), an energy gauge and redox sensor, controls the cell cycle and protects against DNA damage. However, the molecular mechanisms by which AMPKα isoform regulates DNA damage remain largely unknown. The aim of this study was to determine if AMPKα deletion contributes to cellular hyperproliferation by reducing p21(WAF1/Cip1) (p21) expression thereby leading to accumulated DNA damage. The markers for DNA damage, cell cycle proteins, and apoptosis were monitored in cultured mouse embryonic fibroblasts (MEFs) isolated from wild type (WT, C57BL/6J), AMPKα1, or AMPKα2 homozygous deficient (AMPKα1(-/-), AMPKα2(-/-)) mice by Western blot, flow cytometry, and cellular immunofluorescence staining. Deletion of AMPKα1, the predominant AMPKα isoform, but not AMPKα2 in immortalized MEFs led to spontaneous DNA double-strand breaks (DSB) which corresponded to repair protein p53-binding protein 1 (53BP1) foci formation and subsequent apoptosis. Furthermore, AMPKα1 localizes to chromatin and AMPKα1 deletion down-regulates cyclin-dependent kinase inhibitor, p21, an important protein that plays a role in decreasing the incidence of spontaneous DSB via inhibition of cell proliferation. In addition, AMPKα1 null cells exhibited enhanced cell proliferation. Finally, p21 overexpression partially blocked the cellular hyperproliferation of AMPKα1-deleted MEFs via the inhibition of cyclin-dependent kinase 2 (CDK2). Taken together, our results suggest that AMPKα1 plays a fundamental role in controlling the cell cycle thereby affecting DNA damage and cellular apoptosis.
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