Cupro Cancer Research Results
Cupro, Cuproptosis: Click to Expand ⟱
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Cuproptosis is a recently described form of regulated cell death that is distinct from other types such as apoptosis, necroptosis, and pyroptosis. It is primarily characterized by its direct dependence on copper and its interaction with mitochondrial processes.
-Cuproptosis begins with the intracellular accumulation of copper. This free copper binds directly to lipoylated proteins, which are enzymes involved in important mitochondrial metabolic processes such as the tricarboxylic acid (TCA) cycle.
-Protein Aggregation: The binding of copper to these lipoylated proteins induces their aggregation. This aggregation disrupts normal protein functions and compromises mitochondrial integrity.
Cuproptosis represents a unique form of regulated cell death driven by the accumulation of copper and its consequent interactions with mitochondrial lipoylated proteins.
Cuproptosis depends on the intracellular accumulation of copper, which directly binds lipoylated proteins in the TCA cycle, causing protein aggregation and iron-sulfur cluster degradation.
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Scientific Papers found: Click to Expand⟱
TCA↓, suggesting that copper does not target the ETC directly but rather components of the TCA cycle.
toxicity↝, Copper is a double-edged sword – it is essential as a co-factor for enzymes across the animal kingdom, and yet even modest intracellular concentrations can be toxic
Cupro↑, We therefore propose that this novel cell death mechanism be termed cuproptosis.
Cupro↑, As copper dysregulation is common in cancer cells, targeting copper levels or metabolic pathways can trigger cuproptosis, thereby inhibiting tumor growth and progression.
TumCG↓,
Apoptosis↑, Copper can trigger multiple forms of cell death, including apoptosis, oxidative stress-induced necrosis, autophagy and ferroptosis
ROS↑,
Ferroptosis↑,
ETC↓, . Their disruption impairs the electron transport chain and decreases ATP synthesis and mitochondrial membrane potential (76).
MMP↓,
Ca+2↑, Consequently, mitochondrial energy production decreases, accompanied by increased inner membrane permeability, elevated Ca2+ concentration and the accumulation of ROS (77).
Fenton↑, Cu2+ catalyzes the Fenton-like reaction, generating hydroxyl radicals that initiate oxidative stress, leading to extensive cell damage and death (96)
lipid-P↑, These radicals also induce lipid peroxidation, compromising the integrity and fluidity of cell membranes and increasing membrane permeability (99).
MPT↑,
ATP↓, Excess ROS decrease the mitochondrial membrane potential and ATP synthesis and promote cytochrome c release, ultimately activating caspase cascades and triggering apoptosis
Cyt‑c↑,
Casp↑,
angioG↑, Mechanistically, copper promotes tumor progression through multiple pathways. First, copper stimulates angiogenesis by activating angiogenic factors and enhancing the proliferation and migration of vascular endothelial cells
TumCP↑,
TumCMig↑,
TumCI↑, Second, copper serves as a cofactor for several metalloenzymes, including MMP-9, SOD1, vascular adhesion protein-1 and lysyl oxidase (LOX), all of which are key for cancer invasion and metastasis
TumMeta↑,
DDS↑, tussah silk fibroin (TSF)-based nanoparticles (NPs) use TME-responsive release mechanisms to deliver copper and the cuproptosis-inducing drug ES directly to pancreatic cancer cells.
eff↑, suppressed by the copper chelator TTM, further confirming the mechanism of copper-induced cell death. Furthermore, 2-deoxy-D-glucose, a glycolysis inhibitor, can significantly enhance cuproptosis
eff↑, generate a large number of reactive oxygen species (ROS) when exposed to light, which could be adopted for photodynamic therapy.
Fenton↑, Cu2+ is vulnerable to the reduction to Cu+, allowing Cu to drive the Fenton reaction and produce hydroxyl radicals (·OH).
ROS↑, increasing Cu ions in cancer tissue makes an antitumor impact that mainly involves OS by triggering the Fenton reaction, which can produce ROS
eff↑, compared with other metals (iron, chromium, cobalt and nickel), the Cu-based Fenton reaction can react in wider pH range
mtDam↑, Excessive Cu can induce the toxic level of ROS that may aggravate the mitochondrial ROS, causing mitochondrial damage
BAX↑, Cu-induced ROS increased Bax (pro-apoptotic protein), while Bcl2 (anti-apoptotic protein) was decreased
Bcl-2↓,
MMP↓,
Cyt‑c↑, releasing CytC that activated Caspase3
Casp3↑,
ER Stress↑, Nano-CuO) triggers OS by ROS, thus stimulating endoplasmic reticulum (ER)-stress
CHOP↑, which thereby enhanced the expression of CHOP
Apoptosis↑, and CHOP-induced apoptosis
selectivity↑, In fact, autophagy induced by copper can either protect cells from death or contribute to cell death, depending on autophagic flux, which is associated with the concentration of copper.
eff↑, combining artemisinin (ART) and copper peroxide nanodots to enhance autophagy and ferroptosis that produced highly cancer toxic reaction
Pyro↑, Copper-Based Pyroptosis
Paraptosis↑, Copper-Based Paraptosis
Cupro↑, Copper-Based Cuproptosis
ChemoSen↑, studies suggested that Cu-MOFs might be a robust nanoplatform for enhancing chemotherapy activity of Cu-organic compounds.
eff↑, CuS NPs had the ability to directly target cancer cells and then induce in nucleus by modification of RGD and TAT peptides, thus heating cancer cell to exhaustive apoptosis through 980 nm NIR irradiation
TumCD↑, Copper and its compounds are capable of inducing tumor cell death through various mechanisms of action, including activation of apoptosis signaling pathways by reactive oxygen species (ROS), inhibition of angiogenesis, induction of cuproptosis, and p
Apoptosis↓,
ROS↑,
angioG↑,
Cupro↑,
Paraptosis↑,
eff↑, copper nanoparticles can be used as effective agents in chemodynamic therapy, phototherapy, hyperthermia, and immunotherapy.
eff↓, Elevated copper concentrations may promote tumor growth, angiogenesis, and metastasis by affecting cellular processes
selectivity↑, Copper nanoparticles also can selectively attack cancer cells and spare healthy cells
This selectivity is attributed to the EPR effect, which enables nanoparticles to accumulate in tumor tissue by exploiting leaky blood vessels
DNAdam↑, Copper has been found to induce DNA damage and oxidation through the formation of ROS.
eff↑, Tumor cells suffering from oxygen deficiency often have an increased concentration of CTR-1, which facilitates the transport of copper(I) into the cells
eff↑, The results demonstrate the promising capabilities of 64CuCl2 as a valuable tool for both diagnosis and therapy in various types of cancer
eff↑, nanoparticles have remarkable properties, including a large surface area to volume ratio, excellent compatibility with living organisms, and the ability to generate ROS when exposed to an acidic tumor microenvironment
eff↑, Several studies have shown that copper nanoparticles can be used as effective agents in chemodynamic therapy (CDT)
Fenton↑, CDT is a promising treatment strategy for cancer that utilizes the in situ Fenton reaction, which is activated by endogenous substances, such as GSH and H2O2 without the need for external energy input
H2O2↑, Copper-based substrates have been developed that generate H2O2 internally and function effectively in weakly acidic tumor microenvironments (TME)
eff↑, metal peroxide nanomaterials and offers a promising strategy to improve CDT efficacy
eff↑, Copper nanoparticles can also be used in phototherapy
eff↑, Copper nanoparticles have also shown success in destroying cancer tissue by hyperthermia. This method is a local anticancer treatment in which cells are exposed to high temperatures.
RadioS↑, promising results when used in combination with radiotherapy or chemotherapy for various tumor types.
ChemoSen↑,
eff↑, copper nanoparticles are promising in cancer immunotherapy because they enhance immune-based therapies
*toxicity↝, Copper is a necessary trace mineral for the human body, but high concentrations of copper can be toxic
other↑, Extensive research has shown that cancer cells require an increased copper content to support their rapid growth compared to normal cells
eff↑, Copper nanoparticles can be used to generate heat when exposed to certain wavelengths of light or alternating magnetic fields.
Showing Research Papers: 1 to 4 of 4
* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 4
Pathway results for Effect on Cancer / Diseased Cells:
Redox & Oxidative Stress ⓘ
Fenton↑, 3, Ferroptosis↑, 1, H2O2↑, 1, lipid-P↑, 1, ROS↑, 3,
Mitochondria & Bioenergetics ⓘ
ATP↓, 1, ETC↓, 1, MMP↓, 2, MPT↑, 1, mtDam↑, 1,
Core Metabolism/Glycolysis ⓘ
TCA↓, 1,
Cell Death ⓘ
Apoptosis↓, 1, Apoptosis↑, 2, BAX↑, 1, Bcl-2↓, 1, Casp↑, 1, Casp3↑, 1, Cupro↑, 4, Cyt‑c↑, 2, Ferroptosis↑, 1, Paraptosis↑, 2, Pyro↑, 1, TumCD↑, 1,
Transcription & Epigenetics ⓘ
other↑, 1,
Protein Folding & ER Stress ⓘ
CHOP↑, 1, ER Stress↑, 1,
DNA Damage & Repair ⓘ
DNAdam↑, 1,
Proliferation, Differentiation & Cell State ⓘ
TumCG↓, 1,
Migration ⓘ
Ca+2↑, 1, TumCI↑, 1, TumCMig↑, 1, TumCP↑, 1, TumMeta↑, 1,
Angiogenesis & Vasculature ⓘ
angioG↑, 2,
Drug Metabolism & Resistance ⓘ
ChemoSen↑, 2, DDS↑, 1, eff↓, 1, eff↑, 15, RadioS↑, 1, selectivity↑, 2,
Functional Outcomes ⓘ
toxicity↝, 1,
Total Targets: 41
Pathway results for Effect on Normal Cells:
Functional Outcomes ⓘ
toxicity↝, 1,
Total Targets: 1
Scientific Paper Hit Count for: Cupro, Cuproptosis
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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