Uptake of the anticancer drug cisplatin mediated by the copper transporter Ctr1 in yeast and mammals

By S. Ishida, Jaekwon Lee, D. Thiele, I. Herskowitz. Proceedings of the National Academy of Sciences of the United States of America, 2002

899 citations recorded by the source corpus.

Subfields: Nutrition and Dietetics, Oncology

View Paper: https://www.semanticscholar.org/paper/ce2bd1e41b7fb28d9ea8a1f56bfa4fbf85e0f248

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In Nutrition and Dietetics

1. Guido Kroemer

In Oncology

1. Guido Kroemer
2. L. Galluzzi
3. Oliver Kepp
4. B. Kaina
5. W. Roos
6. Matthew D. Hall
7. Lynn M. Pouliot
8. D. Shen

Citations in the corpus

• Cellular processing of platinum anticancer drugs (2005, background): “Mutation or deletion of the CTR1 gene results in increased cisplatin resistance and reduction of platinum levels in both yeast and mouse cell”
• Cisplatin Resistance: A Cellular Self-Defense Mechanism Resulting from Multiple Epigenetic and Genetic Changes (2012, background): “Ishida et al. (2002) demonstrated that uptake of cisplatin is mediated by the copper transporter Ctr1 in yeast and mammals.”
• Molecular mechanisms of resistance and toxicity associated with platinating agents. (2007, background): “More evidence for the role of copper transport in cisplatin sensitivity is based on the observation that cisplatin and copper are competitive inhibitors for the transport of the other molecule into the cell [31,135] Mouse embryonic fibroblasts (MEF) null for CTR1 provide 3.”
• Cisplatin nephrotoxicity: mechanisms and renoprotective strategies. (2008, background): “Earlier work using cancer cell lines concluded that about half of the cisplatin uptake is due to passive diffusion through the plasma membrane, and the remaining half is mediated by an unknown transporter.22 In 2002, Ishida et al.23 showed that deletion of the Ctr1, a high-affinity copper transporte”
• Mechanisms of Cisplatin Nephrotoxicity (2010, background): “Ctr1 is a copper transporter which was also shown to mediate cisplatin uptake into mammalian cells [66], including ovarian cancer cells [67].”
• Mechanisms of resistance to cisplatin and carboplatin. (2007, background): “The copper transporter CTR1 contributes to platinum ellular uptake [62–66], and CTR1-deficient cells are isplatin-resistant [63].”
• DNA damage-induced cell death: from specific DNA lesions to the DNA damage response and apoptosis. (2013, background): “Cisplatin (cis-diammine-dichloroplatinum (II), cDDP, cis-PtCl2(NH3)2) enters the cells ether through passive diffusion or by active transport by Ctr1 (copper transporter 1) [70] or Oct2 (organic cation transporter 2) [71].”
• Pathophysiology of Cisplatin-Induced Acute Kidney Injury (2014, background): “Deletion of the Ctr1, a high-affinity copper transporter, results in reduced uptake of cisplatin and toxicity in yeast [14].”
• Cisplatin: The first metal based anticancer drug. (2019, background): “Modern studies reveal that copper transporter protein CTR1 is also responsible for cisplatin uptake [48].”
• Molecular mechanisms of cisplatin resistance (2012, background): “Ctr1 / mouse embryonic fibroblasts accumulate much less cisplatin than their wild-type counterparts, and are indeed two- to threefold more resistant to its cytotoxic effects (Ishida et al., 2002; Katano et al., 2002; Holzer et al., 2006).”