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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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| Also known as CP32. Cysteinyl aspartate specific proteinase-3 (Caspase-3) is a common key protein in the apoptosis and pyroptosis pathways, and when activated, the expression level of tumor suppressor gene Gasdermin E (GSDME) determines the mechanism of tumor cell death. As a key protein of apoptosis, caspase-3 can also cleave GSDME and induce pyroptosis. Loss of caspase activity is an important cause of tumor progression. Many anticancer strategies rely on the promotion of apoptosis in cancer cells as a means to shrink tumors. Crucial for apoptotic function are executioner caspases, most notably caspase-3, that proteolyze a variety of proteins, inducing cell death. Paradoxically, overexpression of procaspase-3 (PC-3), the low-activity zymogen precursor to caspase-3, has been reported in a variety of cancer types. Until recently, this counterintuitive overexpression of a pro-apoptotic protein in cancer has been puzzling. Recent studies suggest subapoptotic caspase-3 activity may promote oncogenic transformation, a possible explanation for the enigmatic overexpression of PC-3. Herein, the overexpression of PC-3 in cancer and its mechanistic basis is reviewed; collectively, the data suggest the potential for exploitation of PC-3 overexpression with PC-3 activators as a targeted anticancer strategy. Caspase 3 is the main effector caspase and has a key role in apoptosis. In many types of cancer, including breast, lung, and colon cancer, caspase-3 expression is reduced or absent. On the other hand, some studies have shown that high levels of caspase-3 expression can be associated with a better prognosis in certain types of cancer, such as breast cancer. This suggests that caspase-3 may play a role in the elimination of cancer cells, and that therapies aimed at activating caspase-3 may be effective in treating certain types of cancer. Procaspase-3 is a apoptotic marker protein. Prognostic significance: • High Cas3 expression: Associated with good prognosis and increased sensitivity to chemotherapy in breast, gastric, lung, and pancreatic cancers. • Low Cas3 expression: Linked to poor prognosis and increased risk of recurrence in colorectal, hepatocellular carcinoma, ovarian, and prostate cancers. |
| 1572- | Cu, | Recent Advances in Cancer Therapeutic Copper-Based Nanomaterials for Antitumor 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
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