ArticleCell reports. Medicine2020
Targeting Mitochondrial Complex I Overcomes Chemoresistance in High OXPHOS Pancreatic Cancer.
Article in Cell reports. Medicine, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 106 papers.
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Who cites it
106 citing papers in PubMed, 178 citations in OpenAlex.
- Ionomycin suppresses cancer cell growth by disrupting mitochondrial transcription.FEBS open bio · 2026Article
- Mitochondrial metabolism determines chemotherapy sensitivity in colorectal cancer.Nature metabolism · 2026Article
- Mitochondrial integrated stress response activation creates a therapeutic vulnerability to MCL-1 inhibition in acute myeloid leukemia.Cell death & disease · 2026Article
- First-in-Class Covalent Inhibitors of PFKFB3: Discovery and Characterization in PDAC Models.Journal of medicinal chemistry · 2026Article
- Lysosomal lipid metabolism promotes tumor cell invasion through local energetics and membrane lipid remodeling.bioRxiv : the preprint server for biology · 2026Article
- ICAM2 promotes endocrine resistance via dynein-mediated OXPHOS activation in ER-positive breast cancer.Cell death & disease · 2026Article
- Specialized high-capacity mitochondria fuel cell invasion.Current biology : CB · 2026Article
- Review
- Splice-switching of the oncogenic BCS1L isoform suppresses ovarian cancer progression by disrupting mitochondrial function.Cell death & disease · 2026Article
- Mitophagy in pancreatic cancer: mechanistic insights and implications for novel therapeutic strategies.Cell death discovery · 2026Review
- Impacts of Mitochondrial Status After Neoadjuvant Chemotherapy in Esophageal Squamous Cell Carcinoma Patients.Cancer science · 2026Article
- Review
- Enhancing the Nucleoside Analog Response with Translational Therapeutic Approaches to Overcome Resistance.Cells · 2026Review
- MCJ modulates mitochondrial ETC flux to promote lipid metabolism-driven enhancement of cell proliferation and migration.Cell death & disease · 2026Article
- Immune-Mitochondrial Crosstalk in Pancreatic Adenocarcinoma: Systematic Identification of Prognostic Biomarkers Through Immune Dictionary FrameworkEndocrine, metabolic & immune disorders drug targets · 2026Article
- The lactate-lactylation axis in tumor radioresistance: metabolic, epigenetic, and immune mechanisms with emerging links to RNA regulation.Frontiers in immunology · 2026Review
- Article
- ENO1 Knockdown Impedes Tumour Progression and Promotes Oxidative Phosphorylation in Cutaneous Squamous Cell Carcinoma.Acta dermato-venereologica · 2025Article
- Adaptation of redox metabolism in drug-tolerant persister cells is a vulnerability to prevent relapse in pancreatic cancer.Oncogenesis · 2025Article
- Sustained reductions in valine and isoleucine mediate anti-cancer pharmacological effects of inhibiting amino acid transporter LAT1 in cancer cells.Cancer & metabolism · 2025Article
46 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
18 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Mitochondrial respiration (oxidative phosphorylation, OXPHOS) is an emerging target in currently refractory cancers such as pancreatic ductal adenocarcinoma (PDAC). However, the variability of energetic metabolic adaptations between PDAC patients has not been assessed in functional investigations. In this work, we demonstrate that OXPHOS rates are highly heterogeneous between patient tumors, and that high OXPHOS tumors are enriched in mitochondrial respiratory complex I at protein and mRNA levels. Therefore, we treated PDAC cells with phenformin (complex I inhibitor) in combination with standard chemotherapy (gemcitabine), showing that this treatment is synergistic specifically in high OXPHOS cells. Furthermore, phenformin cooperates with gemcitabine in high OXPHOS tumors in two orthotopic mouse models (xenografts and syngeneic allografts). In conclusion, this work proposes a strategy to identify PDAC patients likely to respond to the targeting of mitochondrial energetic metabolism in combination with chemotherapy, and that phenformin should be clinically tested in appropriate PDAC patient subpopulations.
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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.