ArticleJournal of biological inorganic chemistry : JBIC : a publication of the Society of Biological Inorganic Chemistry2014
Roles of Atox1 and p53 in the trafficking of copper-64 to tumor cell nuclei: implications for cancer therapy.
Article in Journal of biological inorganic chemistry : JBIC : a publication of the Society of Biological Inorganic Chemistry, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.
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Who cites it
31 citing papers in PubMed, 49 citations in OpenAlex.
- The interactions of copper, glutamate, and cuproptosis: insights into brain health and Alzheimer's disease pathology.Biometals : an international journal on the role of metal ions in biology, biochemistry, and medicine · 2026Review
- m6A Modification of ATOX1 Inhibits Acute Myeloid Leukemia Progression by Promoting Cuproptosis.Cancer research communications · 2026Article
- Adipose-derived mesenchymal stem cell exosomes ameliorate copper metabolism dysregulation and reduce cuproptosis caused by liver IRI.Frontiers in veterinary science · 2026Article
- Human CTR1 Through the Ages: Milestones and Emerging Roles in Disease and Therapy.Biomolecules · 2025Review
- Preclinical Theranostic Profiling of [Molecules (Basel, Switzerland) · 2025Article
- Copper and hepatic lipid dysregulation: Mechanisms and implications.World journal of hepatology · 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
- Copper metabolism in hepatocellular carcinoma: from molecular mechanisms to therapeutic opportunities.Frontiers in molecular biosciences · 2025Review
- Atox1-cyclin D1 loop activity is critical for survival of tumor cells with inactivated TP53.Bioscience reports · 2024Article
- Copper in colorectal cancer: From copper-related mechanisms to clinical cancer therapies.Clinical and translational medicine · 2024Review
- Regulation of anti-tumor immunity by metal ion in the tumor microenvironment.Frontiers in immunology · 2024Review
- Copper metabolism in osteoarthritis and its relation to oxidative stress and ferroptosis in chondrocytes.Frontiers in molecular biosciences · 2024Review
- Copper metabolism in cell death and autophagy.Autophagy · 2023Review
- Copper chaperone antioxidant 1: multiple roles and a potential therapeutic target.Journal of molecular medicine (Berlin, Germany) · 2023Review
- Identification and validation of a novel cuproptosis-related genes signature associated with prognosis, clinical implications and immunotherapy of hepatocellular carcinoma.Frontiers in pharmacology · 2023Article
- Cellular lethal damage ofFrontiers in medicine · 2023Article
- Editorial:Frontiers in medicine · 2023Article
- The p53 protein is a suppressor of Atox1 copper chaperon in tumor cells under genotoxic effects.PloS one · 2023Article
- Recent Advances in Copper-Based Organic Complexes and Nanoparticles for Tumor Theranostics.Molecules (Basel, Switzerland) · 2022Review
- Article
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4 authors at 3 institutions in 1 country.
Funding
Abstract
Owing to its cytotoxicity, free copper is chelated by protein side chains and does not exist in vivo. Several chaperones transport copper to various cell compartments, but none have been identified that traffic copper to the nucleus. Copper-64 decays by β (+) and β (-) emission, allowing positron emission tomography and targeted radionuclide therapy for cancer. Because the delivery of (64)Cu to the cell nucleus may enhance the therapeutic effect of copper radiopharmaceuticals, elucidation of the pathway(s) involved in transporting copper to the tumor cell nucleus is important for optimizing treatment. We identified Atox1 as one of the proteins that binds copper in the nucleus. Mouse embryonic fibroblast cells, positive and negative for Atox1, were used to determine the role of Atox1 in (64)Cu transport to the nucleus. Mouse embryonic fibroblast Atox1(+/+) cells accumulated more (64)Cu in the nucleus than did Atox1(-/-) cells. HCT 116 colorectal cancer cells expressing p53 (+/+) and not expressing p53 (-/-) were used to evaluate the role of this tumor suppressor protein in (64)Cu transport. In cells treated with cisplatin, the uptake of (64)Cu in the nucleus of HCT 116 p53(+/+) cells was greater than that in HCT 116 p53(-/-) cells. Atox1 expression increased in HCT 116 p53(+/+) and p53(-/-) cells treated with cisplatin; however, Atox1 localized to the nuclei of p53(+/+) cells more than in the p53(-/-) cells. The data presented here indicate that Atox1 is involved in copper transport to the nucleus, and cisplatin affects nuclear transport of (64)Cu in HCT 116 cells by upregulating the expression and the nuclear localization of Atox1.
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