ArticleThe Journal of biological chemistry2009
Functional interactions of Cu-ATPase ATP7B with cisplatin and the role of ATP7B in the resistance of cells to the drug.
Article in The Journal of biological chemistry, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.
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Who cites it
37 citing papers in PubMed, 68 citations in OpenAlex.
- Cuproptosis and the bioinorganic basis of copper-induced cell death.Journal of biological inorganic chemistry : JBIC : a publication of the Society of Biological Inorganic Chemistry · 2026Review
- Multiscale computational genomics in Wilson disease: from atomic dynamics to clinical prediction.Frontiers in genetics · 2026Review
- Copper Homeostasis, Emerging Central Players in Cancer Immunotherapy.Journal of cellular and molecular medicine · 2025Review
- Regulation of the apico-basolateral trafficking polarity of the homologous copper-ATPases ATP7A and ATP7B.Journal of cell science · 2024Article
- The role of metal ions in the occurrence, progression, drug resistance, and biological characteristics of gastric cancer.Frontiers in pharmacology · 2024Review
- Unveiling the genomic landscape of possible metastatic malignant transformation of teratoma secondary to cisplatin-chemotherapy: a Tempus gene analysis-based case report literature review.Frontiers in oncology · 2023Article
- Targeting the Copper Transport System to Improve Treatment Efficacies of Platinum-Containing Drugs in Cancer Chemotherapy.Pharmaceuticals (Basel, Switzerland) · 2021Review
- Oncolytic HSV Therapy Modulates Vesicular Trafficking Inducing Cisplatin Sensitivity and Antitumor Immunity.Clinical cancer research : an official journal of the American Association for Cancer Research · 2021Article
- An integrated analysis of enhancer RNAs in glioma and a validation of their prognostic values.American journal of translational research · 2021Article
- Molecular Bases of Mechanisms Accounting for Drug Resistance in Gastric Adenocarcinoma.Cancers · 2020Review
- Bismuth Porphyrin Antagonizes Cisplatin-Induced Nephrotoxicity via Unexpected Metallothionein-Independent Mechanisms.iScience · 2020Article
- Expression profile and bioinformatics analysis of COMMD10 in BALB/C mice and human.Cancer gene therapy · 2020Article
- Copper-dependent ATP7B up-regulation drives the resistance of TMEM16A-overexpressing head-and-neck cancer models to platinum toxicity.The Biochemical journal · 2019Article
- Ammonium tetrathiomolybdate enhances the antitumor effect of cisplatin via the suppression of ATPase copper transporting beta in head and neck squamous cell carcinoma.Oncology reports · 2019Article
- ATP7B Binds Ruthenium(II)Inorganic chemistry · 2019Article
- Gambogic acid reverses oxaliplatin resistance in colorectal cancer by increasing intracellular platinum levels.Oncology letters · 2018Article
- Modulating Chemosensitivity of Tumors to Platinum-Based Antitumor Drugs by Transcriptional Regulation of Copper Homeostasis.International journal of molecular sciences · 2018Review
- Organic cation transporter 3 mediates cisplatin and copper cross-resistance in hepatoma cells.Oncotarget · 2018Article
- Article
- The role of copper transporter ATP7A in platinum-resistance of esophageal squamous cell cancer (ESCC).Journal of Cancer · 2016Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 2 countries.
Funding
Abstract
Cisplatin is a widely used chemotherapeutic agent for treatment of ovarian, testicular, lung, and stomach cancers. The initial response to the drug is robust; however, tumor cells commonly develop resistance to cisplatin, which complicates treatment. Recently, overexpression of the Cu-ATPase ATP7B in ovary cells was linked to the increased cellular resistance to cisplatin; and the role for Cu-ATPases in the export of cisplatin from cells was proposed. Our results support functional interactions between cisplatin and ATP7B but argue against the active transport through the copper translocation pathway as a mechanism of drug resistance. In hepatocytes, we observed no correlation between the levels of endogenous ATP7B and the resistance of cells to cisplatin. Unlike copper, cisplatin does not induce trafficking of ATP7B in hepatoma cells, neither does it compete with copper in a transport assay. However, cisplatin binds to ATP7B and stimulates catalytic phosphorylation with EC(50) similar to that of copper. Mutations of the first five N-terminal copper-binding sites of ATP7B do not inhibit the cisplatin-induced phosphorylation of ATP7B. In contrast, the deletion of the first four copper-binding sites abolishes the effect of cisplatin on the ATP7B activity. Thus, cisplatin binding to ATP7B and/or general changes in cellular copper homeostasis are likely contributors to the increased resistance to the drug. The link between changes in copper homeostasis and cisplatin resistance was confirmed by treating the Huh7 cells with copper chelator and increasing their resistance to cisplatin.cisplatin.
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