ArticleCell death & disease2020
Oxidized ATM promotes breast cancer stem cell enrichment through energy metabolism reprogram-mediated acetyl-CoA accumulation.
Article in Cell death & disease, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 31 citations in OpenAlex.
- ACLY alleviates cerebral ischemia/reperfusion injury by reducing oxidative stress and enhancing mitochondrial function via histone acetylation.Cell death & disease · 2026Article
- Unraveling the triad of hypoxia, cancer cell stemness, and drug resistance.Journal of hematology & oncology · 2025Review
- Micro-RNAs in breast cancer progression and metastasis: A chromatin and metabolic perspective.Heliyon · 2024Review
- Fatty Acid Oxidation Supports Lymph Node Metastasis of Cervical Cancer via Acetyl-CoA-Mediated Stemness.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Article
- Iron metabolism: backfire of cancer cell stemness and therapeutic modalities.Cancer cell international · 2024Review
- Interplay between epigenetics and metabolism controls cancer stem cell plasticity.Frontiers in epigenetics and epigenomics · 2024Review
- Metabolite itaconate in host immunoregulation and defense.Cellular & molecular biology letters · 2023Review
- Cancer stem cell fate determination: mito-nuclear communication.Cell communication and signaling : CCS · 2023Review
- Nanomaterial-assisted CRISPR gene-engineering - A hallmark for triple-negative breast cancer therapeutics advancement.Materials today. Bio · 2022Review
- Abnormal lipid synthesis as a therapeutic target for cancer stem cells.World journal of stem cells · 2022Review
- Hypoxia Enhances HIF1Stem cells international · 2022Article
- Immune Checkpoint Inhibitors in Tumors Harboring Homologous Recombination Deficiency: Challenges in Attaining Efficacy.Frontiers in immunology · 2022Review
- Acetyl-CoA: An interplay between metabolism and epigenetics in cancer.Frontiers in molecular medicine · 2022Review
- Oxygen and metabolic reprogramming in the tumor microenvironment influences metastasis homing.Cancer biology & therapy · 2021Review
- THOC2 and THOC5 Regulate Stemness and Radioresistance in Triple-Negative Breast Cancer.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2021Article
- Beyond the Double-Strand Breaks: The Role of DNA Repair Proteins in Cancer Stem-Cell Regulation.Cancers · 2021Review
- Harnessing Metabolic Reprogramming to Improve Cancer Immunotherapy.International journal of molecular sciences · 2021Review
- Vasculogenic Mimicry Formation Predicts Tumor Progression in Oligodendroglioma.Pathology oncology research : POR · 2021Article
- Aberrant Metabolism as Inductor of Epigenetic Changes in Breast Cancer: Therapeutic Opportunities.Frontiers in oncology · 2021Review
- Role of Intra- and Extracellular Lipid Signals in Cancer Stemness and Potential Therapeutic Strategy.Frontiers in pharmacology · 2021Review
Corrections and comments
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Authors and funding
13 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cancer stem cell (CSC) is a challenge in the therapy of triple-negative breast cancer (TNBC). Intratumoral hypoxia is a common feature of solid tumor. Hypoxia may contribute to the maintenance of CSC, resulting in a poor efficacy of traditional treatment and recurrence of TNBC cases. However, the underlying molecular mechanism involved in hypoxia-induced CSC stemness maintenance remains unclear. Here, we report that hypoxia stimulated DNA double-strand breaks independent of ATM kinase activation (called oxidized ATM in this paper) play a crucial role in TNBC mammosphere formation and stemness maintenance by governing a specific energy metabolism reprogramming (EMR). Oxidized ATM up-regulates GLUT1, PKM2, and PDHa expressions to enhance the uptake of glucose and production of pyruvate rather than lactate products, which facilitates glycolytic flux to mitochondrial pyruvate and citrate, thus resulting in accumulation of cytoplasmic acetyl-CoA instead of the tricarboxylic acid (TCA) cycle by regulating ATP-citrate lyase (ACLY) activity. Our findings unravel a novel model of TNBC-CSC glucose metabolism and its functional role in maintenance of hypoxic TNBC-CSC stemness. This work may help us to develop new therapeutic strategies for TNBC treatment.
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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.