Copper Cancer Research Results

Copper, Copper: Click to Expand ⟱
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Copper is an essential trace element that plays a critical role in various biological processes, including iron metabolism, energy production, and the functioning of the immune system. However, its relationship with cancer is complex, as both copper deficiency and excess can influence cancer development and progression.
Many cancer cells exhibit elevated levels of copper compared to normal cells. This accumulation can support tumor growth and metastasis by:
Enhancing angiogenesis (the formation of new blood vessels).
Promoting cell proliferation and survival.
Supporting the activity of copper-dependent enzymes that facilitate tumor progression. Copper and Oxidative Stress: While copper is essential for antioxidant enzymes, excess copper can lead to the generation of reactive oxygen species (ROS), contributing to oxidative stress.
Elevated copper levels can promote inflammation and support the growth of tumors.
Copper Chelation Therapy: Given the role of copper in cancer progression, copper chelation (the use of agents that bind copper and promote its excretion) has been explored as a potential therapeutic strategy.
Scientific Papers found: Click to Expand⟱
6237- CUSP9,    CUSP9* treatment protocol for recurrent glioblastoma: aprepitant, artesunate, auranofin, captopril, celecoxib, disulfiram, itraconazole, ritonavir, sertraline augmenting continuous low dose temozolomide
- NA, GBM, NA
PI3K↓, ARTESUNATE phosphoinositide 3-kinase, Akt, increases ROS, NF-κB activation, TNF-alpha, IL-6, TLR2,
Akt↓,
ROS↑,
NF-kB↓,
TNF-α↓,
TLR2↓,
other↓, APREPITANT 10 hrs NK-1 receptors
TrxR↓, AURANOFIN 10 days thioredoxin, increases ROS, STAT3
STAT3↓,
MMPs↓, CAPTOPRIL 2 hrs ACE, AT1 receptors, MMPs
COX1↓, CELECOXIB 9 hrs COX-1 and -2, carbonic anhydrase -2 and -9
COX2↓,
CA↓,
ALDH↓, DISULFIRAM ALDH, increases ROS
P-gp↓, ITRACONAZOLE P-gp efflux transporters, BCRP, Hedgehog, 5-lipoxygenase
HH↓,
5LO↓,
mTOR↓, RITONAVIR P-gp efflux transporters [weak], Akt, mTOR, cyclin D3, proteasome,
CycD3↓,
Proteasome↓,
other↓, SERTRALINE Akt, mTOR, TCTP
MMP2↓, Captopril inhibited the activity of soluble MMP-2 and MMP-9
MMP9↓,
ALDH↓, Disulfiram potent inhibitor of all isoforms of aldehyde dehydrogenase, ALDH, disulfiram stops ethanol metabolism at the acetaldehyde stage
Copper↓, Since disulfiram chelates Cu++ in the stomach even without adding exogenous Cu

1777- MEL,    Melatonin as an antioxidant: under promises but over delivers
- Review, NA, NA
*ROS↓, uncommonly effective in reducing oxidative stress under a remarkably large number of circumstances
*Fenton↓, reportedly chelates transition metals, which are involved in the Fenton/Haber-Weiss reactions
*antiOx↑, credible evidence to suggest that melatonin should be classified as a mitochondria-targeted antioxidant
*toxicity∅, uncommonly high-safety profile of melatonin also bolsters this conclusion.
*GPx↑, melatonin was found to stimulate antioxidative enzymes including glutathione peroxidase and glutathione reductase
*GSR↑,
*GSH↑, melatonin upregulates the synthesis of glutathione
*NO↓, neutralize nitrogen-based toxicants, i.e., nitric oxide
*Iron↓, Melatonin chelates both iron (III) and iron (II), which is the form that participates in the Fenton reaction to generate the hydroxyl radical
*Copper↓, copper-chelating ability of melaton
*IL1β↓, significant reductions in plasma cardiac troponin 1, interleukin 1 beta, inducible nitric oxide synthase (iNOS) and caspase 3 due to melatonin
*iNOS↓,
*Casp3↓,
*BBB↑, melatonin readily crosses the blood-brain barrier;
*RenoP↑, Published reports haveshown that the lung,231, 232 liver, 233- 235 kidney,236 pancreas,237 intestine,238 urinary bladder,239,240 corpus cavernosum,241 skeletal muscle242, 243 spinal cord244, 245 and stem cells246 are alsoprotected by melatonin.
chemoP↑, Melatonin has not been found to interfere with the efficacy of prescription drugs. Doxorubicin, if given it in combination with melatonin may allow the use of a larger dose with greater efficacy.
*Ca+2↝, Moreover, melatonin regulates free Ca2+ movement intracellularly
eff↑, elatonin was found to exaggerate the cancer inhibiting actions of pitavastatin270 and pravastatin271 against breast cancer in experimental studies
*PKCδ?, major targets by which melatonin reduces methamphetamine-related neuronal damage is due to the inhibition of the PKCδ gene
ChemoSen↑, at least some cases melatonin reduces the toxicity of these pharmacological agents in normal cells256, 289, 290 while enhancing the cancer-killing actions (also, see below) of conventional chemotherapeutic agents.256, 291-293
eff↑, TRAIL was combined with melatonin for the treatment of A172 and U87 human glioblastoma cells, however, apoptotic cell death was greatly exaggerated over that caused by TRAIL alone
Akt↓, in GBM: observed effect was related to a modulation of protein kinase c which reduced Akt activation resulting in a rise in death receptor 5 (DR5) levels;
DR5↑,
selectivity↑, The pro-oxidant action of melatonin is common in cancer cells while in normal cells the indoleamine is a powerful antioxidant.
ROS↑, cancer cells
eff↑, human lung adenocarcinoma cells (SK-LV-1) showed that melatonin also increased their sensitivity to the chemotherapy, cisplatin.

2343- QC,    Pharmacological Activity of Quercetin: An Updated Review
- Review, Nor, NA
*ROS↓, Quercetin is a potent scavenger for ROS and hence protects the body against oxidative stress
*GSH↑, Studies of animals and cells have shown that the synthesis of GSH is induced by quercetin.
*Catalase↑, increased expression of superoxide dismutase (SOD), catalase (CAT), and GSH has been reported with the pretreatment of quercetin
*SOD↑,
*MDA↓, quercetin supplementation to layer chickens significantly reduced malondialdehyde (MDA) levels in the kidneys, liver, and heart and increased GSH, CAT, and glutathione peroxidase (GSH-Px) activities in the liver, kidney, and heart tissue
*GPx↑,
*Copper↓, In addition, quercetin can exert antioxidant effects by chelating Cu2+ and Fe2+ in its structure with catechol
*Iron↓,
Apoptosis↓, Quercetin inhibits the proliferation of liver cancer cells via induction of apoptosis and cell cycle arrest [43].
TumCCA↑,
MMP2↓, In HSC-6, SCC-9 human oral cancer cell lines, quercetin inhibits cell viability, migration, and invasion, reduces MMP-2 and MMP-9 abundance, downgrades miR-16, and upgrades HOXA10
MMP9↓,
GlucoseCon↓, quercetin inhibits the mobility of cancer cells by inhibiting glucose uptake and lactic acid production and reducing levels of PKM2, GLUT1, and LDHA, which may have a significant role in controlling breast cancer [56].
lactateProd↓,
PKM2↓,
GLUT1↓,
LDHA↓,
ROS↑, Quercetin encapsulated in solid lipid nanoparticles ,MCF-7 and MCF-10A cells, Increase (ROS)

6174- TM,    Tetrathiomolybdate-associated copper depletion decreases circulating endothelial progenitor cells in women with breast cancer at high risk of relapse
- Trial, BC, NA
OS↑, The 10-month relapse-free survival was 85.0%
toxicity↓, TM is safe and appears to maintain EPCs below baseline in copper-depleted patients.
AntiTum↑, TM may promote tumor dormancy and ultimately prevent relapse.
Copper↓, Tetrathiomolybdate (TM), an oral copper chelator developed for the treatment of Wilson's disease, blocks angiogenesis
angioG↓,

6172- TM,    Phase II trial of copper depletion with tetrathiomolybdate as an antiangiogenesis strategy in patients with hormone-refractory prostate cancer
- Trial, Pca, NA
Copper↓, Seventeen of 19 patients achieved copper deficiency on TM therapy
angioG∅, There was no correlation between prostate-specific antigen and levels of angiogenesis factors.
eff∅, Copper depletion with TM did not delay disease progression in patients with asymptomatic metastatic HRPC.


Showing Research Papers: 1 to 5 of 5

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 5

Pathway results for Effect on Cancer / Diseased Cells:


Redox & Oxidative Stress ⓘ

Copper↓, 3,   ROS↑, 3,   TrxR↓, 1,  

Core Metabolism/Glycolysis ⓘ

GlucoseCon↓, 1,   lactateProd↓, 1,   LDHA↓, 1,   PKM2↓, 1,  

Cell Death ⓘ

Akt↓, 2,   Apoptosis↓, 1,   DR5↑, 1,   Proteasome↓, 1,  

Transcription & Epigenetics ⓘ

other↓, 2,  

Cell Cycle & Senescence ⓘ

CycD3↓, 1,   TumCCA↑, 1,  

Proliferation, Differentiation & Cell State ⓘ

ALDH↓, 2,   HH↓, 1,   mTOR↓, 1,   PI3K↓, 1,   STAT3↓, 1,  

Migration ⓘ

5LO↓, 1,   CA↓, 1,   MMP2↓, 2,   MMP9↓, 2,   MMPs↓, 1,  

Angiogenesis & Vasculature ⓘ

angioG↓, 1,   angioG∅, 1,  

Barriers & Transport ⓘ

GLUT1↓, 1,   P-gp↓, 1,  

Immune & Inflammatory Signaling ⓘ

COX1↓, 1,   COX2↓, 1,   NF-kB↓, 1,   TLR2↓, 1,   TNF-α↓, 1,  

Drug Metabolism & Resistance ⓘ

ChemoSen↑, 1,   eff↑, 3,   eff∅, 1,   selectivity↑, 1,  

Functional Outcomes ⓘ

AntiTum↑, 1,   chemoP↑, 1,   OS↑, 1,   toxicity↓, 1,  
Total Targets: 41

Pathway results for Effect on Normal Cells:


Redox & Oxidative Stress ⓘ

antiOx↑, 1,   Catalase↑, 1,   Copper↓, 2,   Fenton↓, 1,   GPx↑, 2,   GSH↑, 2,   GSR↑, 1,   Iron↓, 2,   MDA↓, 1,   ROS↓, 2,   SOD↑, 1,  

Cell Death ⓘ

Casp3↓, 1,   iNOS↓, 1,  

Migration ⓘ

Ca+2↝, 1,   PKCδ?, 1,  

Angiogenesis & Vasculature ⓘ

NO↓, 1,  

Barriers & Transport ⓘ

BBB↑, 1,  

Immune & Inflammatory Signaling ⓘ

IL1β↓, 1,  

Functional Outcomes ⓘ

RenoP↑, 1,   toxicity∅, 1,  
Total Targets: 20

Scientific Paper Hit Count for: Copper, Copper
2 tetrathiomolybdate
1 CUSP9
1 Melatonin
1 Quercetin
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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