ArticleCell metabolism2019
PML-Regulated Mitochondrial Metabolism Enhances Chemosensitivity in Human Ovarian Cancers.
Article in Cell metabolism, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 195 papers, 2 of them syntheses that pooled it.
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Who cites it
195 citing papers in PubMed, 2 syntheses or guidelines pooled it.
- A multimodal atlas of tumour metabolism reveals the architecture of gene-metabolite covariation.Nature metabolism · 2023Pooled it
- Overlapping gene dependencies for PARP inhibitors and carboplatin response identified by functional CRISPR-Cas9 screening in ovarian cancer.Cell death & disease · 2022Pooled it
- Metabolic vulnerabilities in ovarian cancer decoding the nexus between nutrient adaptation and therapy resistance.Journal of advanced research · 2026Review
- PGC1α-mediated upregulation of PHD2 represses HIF-signaling, limiting prostate cancer progression.Cell death and differentiation · 2026Article
- Pml loss worsens NEK1-linked ALS and Pml induction drives NEK1 degradation, precluding disease onset.The FEBS journal · 2026Article
- Nuclear localization of the glutaminyl-tRNA synthetase QARS reveals its role in DNA damage response in ovarian cancer.Nature communications · 2026Article
- Carboxylesterase 1 is a core metabolic vulnerability of platinum-resistant high-grade serous ovarian carcinoma.Journal of experimental & clinical cancer research : CR · 2026Article
- LSD1-GLS2 axis drives subtype-specific chemoresistance in pancreatic cancer through glutaminolysis reprogramming.Cell death & disease · 2026Article
- Molecular classification identifies aggressive gastrointestinal stromal tumor subtype targetable by PARP inhibitors.Cellular oncology (Dordrecht, Netherlands) · 2026Article
- Boron-Doped Carbon Dots for Organelle Labeling and Mitochondrial Bioimaging.Methods and protocols · 2026Article
- Translating ferroptosis into oncology: challenges, opportunities and future directions.Nature reviews. Clinical oncology · 2026Review
- CSIE: cancer subtyping via inference and ensemble.Briefings in bioinformatics · 2026Article
- Metabolic reprogramming and cisplatin resistance: the emerging role of Pyruvate Dehydrogenase Kinases (PDKs).Cell communication and signaling : CCS · 2026Review
- Splice-switching of the oncogenic BCS1L isoform suppresses ovarian cancer progression by disrupting mitochondrial function.Cell death & disease · 2026Article
- A bioinformatics approach to identify potential biomarkers of high-grade ovarian cancer.Journal of the Turkish German Gynecological Association · 2026Article
- Cell-intrinsic and tumor microenvironmental determinants of platinum resistance in epithelial ovarian cancer.Discover oncology · 2026Review
- Impairment of oxidative metabolism compromises Rad51 recruitment and potentiates PARP inhibitor effectiveness in ovarian cancer.Journal of experimental & clinical cancer research : CR · 2026Article
- Integrative network toxicology and molecular docking reveal epigenetic and endocrine-disrupting mechanisms of PFAS in ovarian cancer.Frontiers in pharmacology · 2026Article
- Mitochondrial metabolic reprogramming at the interface of chemoresistance and immune-cold tumor states.Frontiers in immunology · 2026Review
- Single-Cell Transcriptome Analysis Reveals IRF1-Driven Epithelial States and Glycosaminoglycan-Glycolysis Coupling in Cisplatin-Resistant HGSOC.Cancer informatics · 2026Article
135 more citing papers are in PubMed but not listed here.
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Authors and funding
18 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
High-grade serous ovarian cancer (HGSOC) remains an unmet medical challenge. Here, we unravel an unanticipated metabolic heterogeneity in HGSOC. By combining proteomic, metabolomic, and bioergenetic analyses, we identify two molecular subgroups, low- and high-OXPHOS. While low-OXPHOS exhibit a glycolytic metabolism, high-OXPHOS HGSOCs rely on oxidative phosphorylation, supported by glutamine and fatty acid oxidation, and show chronic oxidative stress. We identify an important role for the PML-PGC-1α axis in the metabolic features of high-OXPHOS HGSOC. In high-OXPHOS tumors, chronic oxidative stress promotes aggregation of PML-nuclear bodies, resulting in activation of the transcriptional co-activator PGC-1α. Active PGC-1α increases synthesis of electron transport chain complexes, thereby promoting mitochondrial respiration. Importantly, high-OXPHOS HGSOCs exhibit increased response to conventional chemotherapies, in which increased oxidative stress, PML, and potentially ferroptosis play key functions. Collectively, our data establish a stress-mediated PML-PGC-1α-dependent mechanism that promotes OXPHOS metabolism and chemosensitivity in ovarian cancer.
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