ArticleCell metabolism2017
MYC and MCL1 Cooperatively Promote Chemotherapy-Resistant Breast Cancer Stem Cells via Regulation of Mitochondrial Oxidative Phosphorylation.
Article in Cell metabolism, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 395 papers.
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The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
395 citing papers in PubMed, 628 citations in OpenAlex.
- Oxidative Phosphorylation Is a Metabolic Vulnerability of Endocrine Therapy-Tolerant Persister Cells in ER+ Breast Cancer.Cancer research · 2025Trial
- Mitochondria-targeted MXene-based nanozymes promote mitophagy and inhibit mtDNA-triggered cGAS/STING inflammation in osteoarthritis.Bioactive materials · 2026Article
- KDM6A loss enhances oxidative phosphorylation uncovering tissue-level convergent evolution.The EMBO journal · 2026Article
- Elesclomol-mediated cuproptosis overcomes cisplatin resistance by restricting epigenetically activated mitochondrial respiration: Novel therapeutic insights into cisplatin-elesclomol combination therapy.Acta pharmaceutica Sinica. B · 2026Article
- Metabolism, autophagy, and cell death: The triangular axis in tumor survival and therapeutic resistance.Redox biology · 2026Review
- Tumor-Intrinsic DNA Damage Signaling Is Associated with MHC-I Expression and CD8 Cytotoxic T-Cell Engagement in Triple-Negative Breast Cancer.Current issues in molecular biology · 2026Article
- Integrated Multiomic Profiling Enhances Risk Stratification and Prognostication in Canine Osteosarcoma.Clinical cancer research : an official journal of the American Association for Cancer Research · 2026Article
- Oxidative Phosphorylation and Fatty Acid Oxidation Are Central to Mitochondrial Metabolism Rewiring in CML Stem/Progenitor Cell Survival.Pathophysiology : the official journal of the International Society for Pathophysiology · 2026Review
- Homer3 Promotes Aggressive Phenotypes in Triple-Negative Breast Cancer Through Cell Cycle- and MYC-Associated Programs.International journal of molecular sciences · 2026Article
- HIFs: The central drivers of tumors and their role as molecular switches in targeted therapy?Acta pharmaceutica Sinica. B · 2026Review
- MYC Addiction as a Targetable Vulnerability in Nelarabine-Resistant T-Cell Acute Lymphoblastic Leukemia.Cancer science · 2026Article
- Nanotechnology in triple-negative breast cancer: a review of nanocarrier systems for enhanced efficacy and reduced toxicity.Nanoscale advances · 2026Review
- PLSCR1 drives chemoresistance in TNBC via METTL3/IGF2BP3-mediated mRNA stabilization and EGFR-MAPK pathway activation.Cell death & disease · 2026Article
- Complex I protein NDUFB9 is a metabolic vulnerability in triple negative breast cancer brain metastases.Nature communications · 2026Article
- TENT5A Maintains MYC mRNA Stability to Enhance Osteosarcoma Stemness.Cancer research · 2026Article
- YTHDF3 Mediates the Occurrence and Development of Breast Cancer by Regulating Glycolysis Through the mTOR-HIF1α-LHDA Axis.Journal of cellular and molecular medicine · 2026Article
- ASPP2 inhibits hepatocellular carcinoma growth by regulating cuproptosis via mitochondrial protein lipoylation.Cell death & disease · 2026Article
- Review
- Metabolic Response to CDK4/6 Inhibition in ER+ Breast Cancer Creates a Therapeutic Vulnerability in Drug-Tolerant Persister Cells.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026Article
- Early Epigenetic and Metabolic Responses to the Adipocyte Secretome Reveal Stress-Adaptive States in Triple-Negative Breast Cancer.bioRxiv : the preprint server for biology · 2026Article
335 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
19 authors at 5 institutions in 3 countries.
Funding
Abstract
Most patients with advanced triple-negative breast cancer (TNBC) develop drug resistance. MYC and MCL1 are frequently co-amplified in drug-resistant TNBC after neoadjuvant chemotherapy. Herein, we demonstrate that MYC and MCL1 cooperate in the maintenance of chemotherapy-resistant cancer stem cells (CSCs) in TNBC. MYC and MCL1 increased mitochondrial oxidative phosphorylation (mtOXPHOS) and the generation of reactive oxygen species (ROS), processes involved in maintenance of CSCs. A mutant of MCL1 that cannot localize in mitochondria reduced mtOXPHOS, ROS levels, and drug-resistant CSCs without affecting the anti-apoptotic function of MCL1. Increased levels of ROS, a by-product of activated mtOXPHOS, led to the accumulation of HIF-1α. Pharmacological inhibition of HIF-1α attenuated CSC enrichment and tumor initiation in vivo. These data suggest that (1) MYC and MCL1 confer resistance to chemotherapy by expanding CSCs via mtOXPHOS and (2) targeting mitochondrial respiration and HIF-1α may reverse chemotherapy resistance in TNBC.
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What OpenQuestion holds
Registered trials
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.