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| Copper Metal Copper levels are considerably elevated in various malignancies. Copper [Cu(II)] is a transition and trace element in living organisms. It increases reactive oxygen species (ROS) and free-radical generation that might damage biomolecules like DNA, proteins, and lipids. Copper (dietary/physiology) ≠ copper-loading therapeutics ≠ copper nanoparticles. For Cu nanoparticles, the dominant and most reproducible theme is toxicity via ROS → mitochondrial damage/genotoxicity, not clean tumor selectivity. - Copper acts as a critical cofactor for numerous enzymes involved in redox reactions, energy production, and connective tissue formation. - Increased copper levels in the tumor microenvironment can enhance angiogenic signaling and thus supply the tumor with necessary oxygen and nutrients, facilitating tumor growth and metastasis. - Copper can participate in redox cycling reactions, similar to the Fenton reaction, leading to the production of reactive oxygen species (ROS). - Cancer cells often exhibit altered copper homeostasis, with some studies showing elevated copper levels in tumor tissues relative to normal tissues. Two main approaches are: - Copper Chelation: Drugs that bind copper (chelators) can reduce the bioavailability of copper, potentially inhibiting angiogenesis and other copper-dependent tumor processes. - Copper Ionophores: These agents facilitate the transport of copper into cancer cells to induce cytotoxicity by elevating intracellular copper levels beyond a tolerable threshold, leading to cell death. - Depletion of glutathione and stimulation of lipid peroxidation, catalase and superoxide dismutase. - Studies have shown that the level of copper in tumour cells and blood serum from cancer patients is elevated, and the conclusion is that cancer cells need more copper than healthy cells. (but also sometimes depleted). - Copper is a double-edged sword, maintaining normal cell development and promoting tumor development. - Tumor tissue has a higher demand for copper and is more susceptible to copper homeostasis, copper may modulate cancer cell survival through reactive oxygen species (ROS) excessive accumulation, proteasome inhibition and anti-angiogenesis. Natural Product: Cu, Copper (ion biology)
Time-Scale Flag (TSF): P / R / G
Copper Nanoparticles: CuNP / CuO-NP (tox + “anticancer” claims are mostly preclinical)
Time-Scale Flag (TSF): P / R / G
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| The Fenton reaction is a chemical reaction that involves the catalytic decomposition of hydrogen peroxide (H2O2) by iron ions (Fe2+ or Fe3+). This reaction produces highly reactive oxygen species (ROS), including hydroxyl radicals (·OH) and superoxide anions (O2·-). Cancer Progression: Increased oxidative stress from the Fenton reaction can promote cancer cell proliferation, survival, and metastasis. ROS can activate various signaling pathways that support tumor growth and resistance to apoptosis. Therapeutic Target: The Fenton reaction has been explored as a potential therapeutic target. Strategies to manipulate iron levels or enhance the production of ROS in cancer cells are being investigated to selectively induce cell death in tumors. Formula Fe2+ + H2O2 → Fe3+ + HO• + OH− Fe3+ + H2O2 → Fe2+ + HOO• + H+ 2 H2O2 → HO• + HOO• + H2O net reaction – The dysregulation of iron metabolism in certain cancers might serve as a biomarker for targeted treatments that employ Fenton reaction-based strategies. – Researchers are investigating strategies that harness or amplify the Fenton reaction to selectively kill cancer cells. - With more available iron, the Fenton reaction can be enhanced, resulting in increased production of hydroxyl radicals. Which can lead to cancer cell death. See the ROS target for more information |
| 1603- | Cu, | BP, | SDT, | Glutathione Depletion-Induced ROS/NO Generation for Cascade Breast Cancer Therapy and Enhanced Anti-Tumor Immune Response |
| - | in-vitro, | BC, | 4T1 | - | in-vivo, | NA, | NA |
| 1602- | Cu, | A simultaneously GSH-depleted bimetallic Cu(ii) complex for enhanced chemodynamic cancer therapy† |
| - | in-vitro, | BC, | MCF-7 | - | in-vitro, | BC, | 4T1 | - | in-vitro, | Lung, | A549 | - | in-vitro, | Liver, | HepG2 |
| 1596- | Cu, | CDT, | Unveiling the promising anticancer effect of copper-based compounds: a comprehensive review |
| - | Review, | NA, | NA |
| 1572- | Cu, | Recent Advances in Cancer Therapeutic Copper-Based Nanomaterials for Antitumor Therapy |
| - | Review, | NA, | NA |
| 1571- | Cu, | Copper in cancer: From pathogenesis to therapy |
| - | Review, | NA, | NA |
Query results interpretion may depend on "conditions" listed in the research papers. Such Conditions may include : -low or high Dose -format for product, such as nano of lipid formations -different cell line effects -synergies with other products -if effect was for normal or cancerous cells
Filter Conditions: Pro/AntiFlg:% IllCat:% CanType:% Cells:% prod#:64 Target#:804 State#:% Dir#:2
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