ArticleProceedings of the National Academy of Sciences of the United States of America2022
Memo1 binds reduced copper ions, interacts with copper chaperone Atox1, and protects against copper-mediated redox activity in vitro.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers, 1 of them a synthesis that pooled it.
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Who cites it
40 citing papers in PubMed, 1 synthesis or guideline pooled it, 55 citations in OpenAlex.
- Coping with copper: a bibliometric analysis of copper's role in cancer pathogenesis and treatment.Systematic reviews · 2025Pooled it
- From copper imbalance to immunometabolic remodeling: cuproptosis-related vulnerability and therapeutic hypotheses in autoimmune diseases.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026Review
- Integrated genomic and transcriptomic approaches reveal oxidative stress adaptation mechanisms in a mesotrione-resistant Amaranthus tuberculatus biotype.Pest management science · 2026Article
- Article
- ATOX1 alleviates radiation-induced cardiac injury by modulating AMPK/NRF2 to inhibit myocardial oxidative stress and mitochondrial dysfunction.Journal of cell communication and signaling · 2026Article
- Schistosome esophageal gland factor MEG-8.2 drives host cell lysis and interacts with host immune proteins.PLoS pathogens · 2026Article
- Tackling cuproptosis: from metabolic rewiring to therapeutic exploitation in cancer.Cellular & molecular immunology · 2026Review
- Role of Copper Homeostasis and Cuproptosis in Cardiovascular Disease: Molecular Insights and Metabolic Perspectives.International journal of biological sciences · 2026Review
- Chromatin Remodeling Subunit ARID1A Negatively Regulates the Malignant Progression of Gastrointestinal Stromal Tumors by Targeting the MEMO1 Promoter.International journal of medical sciences · 2026Article
- Targeting metalloptosis in tumor therapy: from molecular mechanisms to application of metal nanoparticles.Molecular cancer · 2025Review
- The Regulation of Trace Metal Elements in Cancer Ferroptosis.Advanced biology · 2025Review
- Balancing between cuproplasia and copper-dependent cell death: molecular basis and clinical implications of ATOX1 in cancer.Journal of experimental & clinical cancer research : CR · 2025Review
- Emerging regulated cell death mechanisms in bone remodeling: decoding ferroptosis, cuproptosis, disulfidptosis, and PANoptosis as therapeutic targets for skeletal disorders.Cell death discovery · 2025Review
- Cuproptosis: a novel therapeutic mechanism in lung cancer.Cancer cell international · 2025Review
- The molecular mechanism and therapeutic landscape of copper and cuproptosis in cancer.Signal transduction and targeted therapy · 2025Review
- Targeting cuproptosis for cancer therapy: Focus on the anti-tumor immune system.Cancer pathogenesis and therapy · 2025Review
- Copper is essential for cyclin B1-mediated CDK1 activation.Nature communications · 2025Article
- Cuproptosis: molecular mechanisms, cancer prognosis, and therapeutic applications.Journal of translational medicine · 2025Review
- Biometallic ions and derivatives: a new direction for cancer immunotherapy.Molecular cancer · 2025Review
- Copper metabolism in hepatocellular carcinoma: from molecular mechanisms to therapeutic opportunities.Frontiers in molecular biosciences · 2025Review
Corrections and comments
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Authors and funding
8 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The protein mediator of ERBB2-driven cell motility 1 (Memo1) is connected to many signaling pathways that play key roles in cancer. Memo1 was recently postulated to bind copper (Cu) ions and thereby promote the generation of reactive oxygen species (ROS) in cancer cells. Since the concentration of Cu as well as ROS are increased in cancer cells, both can be toxic if not well regulated. Here, we investigated the Cu-binding capacity of Memo1 using an array of biophysical methods at reducing as well as oxidizing conditions in vitro. We find that Memo1 coordinates two reduced Cu (Cu(I)) ions per protein, and, by doing so, the metal ions are shielded from ROS generation. In support of biological relevance, we show that the cytoplasmic Cu chaperone Atox1, which delivers Cu(I) in the secretory pathway, can interact with and exchange Cu(I) with Memo1 in vitro and that the two proteins exhibit spatial proximity in breast cancer cells. Thus, Memo1 appears to act as a Cu(I) chelator (perhaps shuttling the metal ion to Atox1 and the secretory path) that protects cells from Cu-mediated toxicity, such as uncontrolled formation of ROS. This Memo1 functionality may be a safety mechanism to cope with the increased demand of Cu ions in cancer cells.
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