ArticleNature communications2020
OXPHOS remodeling in high-grade prostate cancer involves mtDNA mutations and increased succinate oxidation.
Article in Nature communications, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 98 papers.
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98 citing papers in PubMed.
- Cancer-associated mitochondrial homeostasis disrupted and retrograde signaling activated.Medical oncology (Northwood, London, England) · 2026Review
- METTL5-mediated rRNA modification controls prostate cancer progression through the IRF7/DNA2 axis and mitophagy regulation.Oncogene · 2026Article
- Mitochondrial DNA mutations are associated with impaired oxidative phosphorylation and enhanced imatinib response in chronic myeloid leukemia.HemaSphere · 2026Article
- Label-free optical biomarker for prostate cancer diagnosis.Molecular medicine (Cambridge, Mass.) · 2026Article
- Redox Homeostasis, Metabolic Pathways and Plasticity in Uveal Melanoma Compared to Other Cancers.Cancers · 2026Review
- Lactylation landscape of mitochondrial proteins in myocardial infarction.Redox biology · 2026Article
- Integrative transcriptomic and single-cell analysis reveals metabolic reprogramming and hexosamine biosynthesis-mediated tumor microenvironment remodeling in prostate cancer.Discover oncology · 2026Article
- HER2-driven mammary tumorigenesis enhances bioenergetics despite reductions in mitochondrial content.eLife · 2026Article
- Lactylation landscape of mitochondrial proteins in myocardial infarction.bioRxiv : the preprint server for biology · 2026Article
- Intermittent Fasting and Androgen Receptor Signaling in Prostate Cancer: Metabolic Crosstalk and Therapeutic Implications.International journal of molecular sciences · 2026Review
- ANOS1 Facilitated Tumorigenesis in Gastric Cancer through the Regulation of Oxidative Phosphorylation Pathway.Journal of microbiology and biotechnology · 2026Article
- Mitochondrial DNA mutations and intercellular mitochondrial transfer in cancer: mechanisms, biological effects, and clinical potential.Biomarker research · 2026Review
- Biomimetic bone niche reconstructs proliferation-inhibited and therapy-resistant bone-metastatic prostate cancer.Bioactive materials · 2026Article
- MCJ modulates mitochondrial ETC flux to promote lipid metabolism-driven enhancement of cell proliferation and migration.Cell death & disease · 2026Article
- Mitochondrial complex I in focus: mechanisms and therapeutic strategies of urinary system diseases.Frontiers in physiology · 2026Review
- Bioenergetic profiles and respiratory control in mitochondrial physiology: Precision analysis of oxidative phosphorylation.Experimental physiology · 2026Article
- The multifaceted roles of mitochondria and their therapeutic transformation: a new perspective on triple-negative breast cancer treatment.Frontiers in oncology · 2026Article
- Targeting SLC25A33 Suppresses Vascular Smooth Muscle Cell Proliferation and Migration by Reducing Cytosolic mtDNA Levels: Implications for Occlusive Vascular Diseases.Diabetes & metabolism journal · 2026Article
- SBFI Inhibitors Reprogram Transcriptomic Landscape of Prostate Cancer Cells Leading to Cell Death.Cancers · 2025Article
- Biological and translational attributes of mitochondrial DNA copy number: Laboratory perspective to clinical relevance.World journal of methodology · 2025Review
38 more citing papers are in PubMed but not listed here.
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17 authors.
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No grant is acknowledged in the PubMed record.
Abstract
Rewiring of energy metabolism and adaptation of mitochondria are considered to impact on prostate cancer development and progression. Here, we report on mitochondrial respiration, DNA mutations and gene expression in paired benign/malignant human prostate tissue samples. Results reveal reduced respiratory capacities with NADH-pathway substrates glutamate and malate in malignant tissue and a significant metabolic shift towards higher succinate oxidation, particularly in high-grade tumors. The load of potentially deleterious mitochondrial-DNA mutations is higher in tumors and associated with unfavorable risk factors. High levels of potentially deleterious mutations in mitochondrial Complex I-encoding genes are associated with a 70% reduction in NADH-pathway capacity and compensation by increased succinate-pathway capacity. Structural analyses of these mutations reveal amino acid alterations leading to potentially deleterious effects on Complex I, supporting a causal relationship. A metagene signature extracted from the transcriptome of tumor samples exhibiting a severe mitochondrial phenotype enables identification of tumors with shorter survival times.
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