ArticleCell death discovery2023
Aurora kinase A/AURKA functionally interacts with the mitochondrial ATP synthase to regulate energy metabolism and cell death.
Article in Cell death discovery, 2023. 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.
- Application and mechanistic research of novel therapeutic strategies in cisplatin-resistant small cell lung cancer.Annals of medicine · 2026Review
- How mitochondrial heterogeneity fuels a dynamic organelle ecosystem.Communications biology · 2026Review
- Combining Fret and Super-Resolution Microscopy Reveals Kinase Activation and Mitochondrial Activity at the Nanoscale.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Cell Cycle Control of Nuclear Metabolism Couples Phosphatidylinositol Signaling to Histone Methylation.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Three-dimensional (3D) culture-primed placental mesenchymal stem cells decrease cellular heterogeneity, significantly enhancing osteogenesis via improving mitochondrial function.Materials today. Bio · 2026Article
- Development of capsaicin-derived prohibitin ligands to modulate the Aurora kinase A/PHB2 interaction and mitophagy in cancer cells.Communications biology · 2026Article
- GLP-1 receptor agonist protects glucose-stimulated insulin secretion in pancreatic β-cells against lipotoxicity via PPARδ/UCP2 pathway.Cellular and molecular life sciences : CMLS · 2025Article
- Aurora kinases signaling in cancer: from molecular perception to targeted therapies.Molecular cancer · 2025Review
- Identification and validation of a metabolic-related gene risk model predicting the prognosis of lung, colon, and breast cancers.Scientific reports · 2025Article
- Exploring genetic signatures of obesity: hub genes and miRNAs unveiled through comprehensive bioinformatic analysis.Journal of diabetes and metabolic disorders · 2024Article
- Article
- Identification of POU4F1 as a novel prognostic biomarker and therapeutic target in esophageal squamous cell carcinoma.Cancer cell international · 2024Article
- The PIN1-YTHDF1 axis promotes breast tumorigenesis via the mArchives of pharmacal research · 2024Article
- Aurora Kinase A: Integrating Insights into Cancer, Inflammation, and Infectious Diseases.Gut microbes reports · 2024Review
- Mitochondrial proteins as therapeutic targets in diabetic ketoacidosis: evidence from Mendelian randomization analysis.Frontiers in pharmacology · 2024Article
Corrections and comments
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Authors and funding
3 authors.
Funding
Abstract
Cancer cells often hijack metabolic pathways to obtain the energy required to sustain their proliferation. Understanding the molecular mechanisms underlying cancer cell metabolism is key to fine-tune the metabolic preference of specific tumors, and potentially offer new therapeutic strategies. Here, we show that the pharmacological inhibition of mitochondrial Complex V delays the cell cycle by arresting breast cancer cell models in the G0/G1 phase. Under these conditions, the abundance of the multifunctional protein Aurora kinase A/AURKA is specifically lowered. We then demonstrate that AURKA functionally interacts with the mitochondrial Complex V core subunits ATP5F1A and ATP5F1B. Altering the AURKA/ATP5F1A/ATP5F1B nexus is sufficient to trigger G0/G1 arrest, and this is accompanied by decreased glycolysis and mitochondrial respiration rates. Last, we discover that the roles of the AURKA/ATP5F1A/ATP5F1B nexus depend on the specific metabolic propensity of triple-negative breast cancer cell lines, where they correlate with cell fate. On one hand, the nexus induces G0/G1 arrest in cells relying on oxidative phosphorylation as the main source of energy. On the other hand, it allows to bypass cell cycle arrest and it triggers cell death in cells with a glycolytic metabolism. Altogether, we provide evidence that AURKA and mitochondrial Complex V subunits cooperate to maintain cell metabolism in breast cancer cells. Our work paves the way to novel anti-cancer therapies targeting the AURKA/ATP5F1A/ATP5F1B nexus to lower cancer cell metabolism and proliferation.
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Registered trials
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