Iron Cancer Research Results

Iron, Iron: Click to Expand ⟱
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Type:
Iron is an essential nutrient that is crucial for various cellular processes, including DNA synthesis, cell proliferation, and oxygen transport.
Cancer cells often have increased iron requirements due to their rapid growth and proliferation. Some tumors can acquire iron through various mechanisms, including upregulating iron transport proteins. This can support their growth and survival.
Excess iron can lead to the production of reactive oxygen species (ROS) through Fenton reactions, which can cause oxidative damage to DNA, proteins, and lipids. This oxidative stress can contribute to cancer development and progression.
Scientific Papers found: Click to Expand⟱
3284- ALA,    Alpha-Lipoic Acid Mediates Clearance of Iron Accumulation by Regulating Iron Metabolism in a Parkinson's Disease Model Induced by 6-OHDA
- vitro+vivo, Park, NA
*antiOx↑, naturally occurring enzyme cofactor with antioxidant and iron chelator properties and has many known effects. ALA has neuroprotective effects on PD.
*IronCh↑,
*neuroP↑,
*ROS↓, decreasing the levels of intracellular reactive oxygen species and iron.
*Iron↓,
*BBB↑, ALA also provides neuroprotection against PD because it can penetrate the blood–brain barrier.
*motorD↑, ALA ameliorates motor behavior and prevents DA neuron loss in the SN of PD rat models.
*GSH↑, ALA Inhibits the Decrease in the Activity of SOD and GSH in the SN of a Rat Model of PD Induced by 6-OHDA

5132- ART/DHA,    Dihydroartemisinin Exerts Its Anticancer Activity through Depleting Cellular Iron via Transferrin Receptor-1
- in-vitro, Liver, HepG2 - in-vitro, BC, MCF-7
Iron↓, In the current study, we found that dihydroartemisinin caused cellular iron depletion in time- and concentration-dependent manners.
TfR1/CD71↓, Moreover, dihydroartemisinin reduced the level of transferrin receptor-1 associated with cell membrane.
ROS↑, which may be a new action mechanism of DHA independently of oxidative damage.

1076- ART/DHA,    The Potential Mechanisms by which Artemisinin and Its Derivatives Induce Ferroptosis in the Treatment of Cancer
- Review, NA, NA
Ferroptosis↑,
ROS↑, interaction between heme-derived iron and ART will result in the production of ROS
ER Stress↑,
i-Iron↓, DHA can cause intracellular iron depletion in a time- and dose-dependent manner
TumAuto↑,
AMPK↑,
mTOR↑,
P70S6K↑,
Fenton↑,
lipid-P↑,
ROS↑,
ChemoSen↑, combination of ART and Nrf2 inhibitors to promote ferroptosis may have more efficient anticancer effects without damaging normal cells.
NRF2↑, Liu et al. discovered that ART covalently targets Keap1 at Cys151 to activate the Nrf2-dependent pathway [94
NRF2↓, inhibition of Nrf2-related gene expression accelerated erastin and sorafenib-induced ferroptosis [45]. More importantly, an accumulating body of research suggests that ART may induce ferroptosis in cancer cells by regulating the above molecules.

5883- CAR,    Safety and tolerability of carvacrol in healthy subjects: a phase I clinical study
- Trial, Nor, NA
*Dose↝, Subjects were randomly divided into two groups receiving 1 and 2 mg/kg/day carvacrol.
*HDL↓, There was significant reductions in high-density lipoprotein cholesterol (HDL), total bilirubin, amylase, iron, red blood cells (RBC) count, and HCT after one-month treatment with 2 mg/kg/day carvacrol
*Bil↓,
*Iron↓,
*toxicity↓, The results of this phase I study regarding carvacrol effects on healthy subjects, showed clinical safety and tolerability for this agent.

1633- HCA,    Hydroxycitric Acid Alleviated Lung Ischemia-Reperfusion Injury by Inhibiting Oxidative Stress and Ferroptosis through the Hif-1α Pathway
- in-vivo, NA, NA - in-vitro, Nor, HUVECs
*other↓, HCA effectively attenuated lung injury, inflammation, and edema induced by ischemia reperfusion
*Inflam↓,
*MDA↓, HCA treatment significantly reduced malondialdehyde (MDA) and reactive oxygen species (ROS) levels
*ROS↓,
*Iron↓, while decreasing iron content and increasing superoxide dismutase (SOD)
*SOD↓,
*Hif1a↓, HCA administration significantly inhibited Hif-1α and HO-1 upregulation both in vivo and in vitro.
*HO-1↓,

4213- Hup,    Huperzine A-Liposomes Efficiently Improve Neural Injury in the Hippocampus of Mice with Chronic Intermittent Hypoxia
- in-vivo, NA, NA
*cognitive↑, HuA-LIP significantly ameliorated cognitive dysfunction and neuronal damage in CIH mice.
*SOD↑, HuA-LIP elevated T-SOD and GSH-Px abilities and decreased MDA content to resist oxidative stress damage induced by CIH.
*GPx↑,
*MDA↓,
*ROS↓,
*Iron↓, HuA-LIP reduced brain iron levels by downregulating TfR1, hepcidin, and FTL expression.
*TfR1/CD71↓,
*FTL↓,
*ERK↑, HuA-LIP activated the PKAα/Erk/CREB/BDNF signaling pathway and elevated MAP2, PSD95, and synaptophysin to improve synaptic plasticity.
*PKA↑,
*CREB↑,
*BDNF↑,
*PSD95↑,
*neuroP↑, HuA-LIP showed a superior performance against neuronal damage induced by CIH.

4209- Hup,    Huperzine A, reduces brain iron overload and alleviates cognitive deficit in mice exposed to chronic intermittent hypoxia
- in-vivo, NA, NA
*ROS↓, HuA improves synaptic plasticity and decreases ROS level in CIH mice
*cognitive↑, HuA significantly improved cognitive impairment and neuronal damage in the hippocampus of CIH mice via increasing the ratio of Bcl-2/Bax and inhibiting caspase-3 cleavage.
*neuroP↑,
*Bax:Bcl2↓,
*Casp3↑,
*NADPH↓, HuA considerably decreased ROS levels by downregulating the high levels of NADPH oxidase (NOX 2, NOX 4) mediated by CIH.
*NOX↓,
*TfR1/CD71↓, Decreased levels of TfR1 and FTL proteins observed in HuA treated CIH group, could reduce iron overload in hippocampus. HuA increased PSD 95 protein expression, CREB activation and BDNF protein expression
*Iron↓,
*PSD95↑,
*BDNF↑,

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)

5026- QC,    Quercetin induces ferroptosis in gastric cancer cells by targeting SLC1A5 and regulating the p-Camk2/p-DRP1 and NRF2/GPX4 Axes
- in-vitro, GC, NA
SLC1A5↓, We demonstrated that Quer inhibits SLC1A5 expression
ROS↑, we found that Quer altered the intracellular ROS levels, antioxidant system protein expression levels, and iron content.
Iron↓, Quer increased the intracellular iron content by inhibiting SLC1A5
NRF2↓, Mechanistically, Quer binds to SLC1A5, inhibiting the nuclear translocation of nuclear factor erythroid 2-related factor 2 (NRF2), resulting in decreased xCT/GPX4 expression.
GPx4↓,
Ferroptosis↑, These three changes collectively led to ferroptosis in GC cells

1748- RosA,    The Role of Rosmarinic Acid in Cancer Prevention and Therapy: Mechanisms of Antioxidant and Anticancer Activity
- Review, Var, NA
AntiCan↑, RA exhibits significant potential as a natural agent for cancer prevention and treatment
*BioAv↝, Various factors, including its lipophilic nature, stability in the gastrointestinal tract, and interactions with food, can significantly influence its absorption
*CardioT↓, RA attenuated these effects by reducing ROS levels, indicating its potential role as a cardioprotective agent during chemotherapy.
*Iron↓, Another significant mechanism antioxidant activity of RA is its capacity to chelate transition metal ions, particularly iron (Fe2+) and copper (Cu2+), which can catalyze the formation of highly reactive hydroxyl radicals through the Fenton reaction.
*ROS↓, forming stable complexes with Fe2+ and Cu2+, thus inhibiting their pro-oxidant activity.
*SOD↑, SOD, CAT, and GPx, play crucial roles in neutralizing ROS and maintaining cellular redox homeostasis. RA upregulates the expression and activity of these enzymes
*Catalase↑,
*GPx↑,
*NRF2↑, activation of the nuclear factor erythroid 2-related factor 2 (Nrf2) pathway, a primary regulator of the antioxidant response
MARK4↓, Anwar’s study demonstrated that RA inhibited MARK4 activity in MDA-MB-231 breast cancer cells, resulting in dose-dependent apoptosis
MMP9↓, RA effectively inhibited cancer cell invasion and migration by reducing matrix metalloproteinase-9 (MMP-9) activity
TumCCA↑, caused cell cycle arrest
Bcl-2↓, RA downregulates Bcl-2 expression and upregulates Bax, thereby promoting apoptosis
BAX↑,
Apoptosis↑,
E-cadherin↑, promoting E-cadherin expression, while downregulating N-cadherin and vimentin
N-cadherin↓,
Vim↓,
Gli1↓, induced apoptosis by downregulating Gli1, a key component of the Hedgehog signaling pathway,
HDAC2↓, RA induced apoptosis by modulating histone deacetylase 2 (HDAC2) expression
Warburg↓, anti-Warburg effect of RA in colorectal carcinoma
Hif1a↓, RA inhibits hypoxia-inducible factor-1 alpha (HIF-1α) and downregulates miR-155
miR-155↓,
p‑PI3K↑, RA has been shown to upregulate p-PI3K, protecting cells through the PI3K/Akt pathway,
ROS↑, RA, induces significant ROS generation in A549 cells, which triggers both apoptosis and autophagy.
*IronCh↑, RA’s dual nature as both a phenolic acid and a flavonoid-related compound enables it to chelate metal ions and prevent the formation of free radicals,

1743- RosA,    New insights into the competition between antioxidant activities and pro-oxidant risks of rosmarinic acid
- Analysis, Var, NA
ROS↑, Finally, the pro-oxidant risk of RA− was also considered via the Fe(iii)-to-Fe(ii) complex reduction process, which may initiate Fenton-like reactions forming reactive HO˙ radicals.
Fenton↑,
eff↑, RA− does not enhance the reduction process when ascorbate anions are present as reducing agents, whereas the pro-oxidant risk becomes remarkable when superoxide anions are found
antiOx↑, The antioxidant activity of RA in this studied system is remarkably higher than that of trolox, ascorbic acid and taxifolin
Iron↓, it is noteworthy that RA− represents strong chelating ability towards both Fe(ii) and Fe(iii) ions compared to its neutral form RA
ROS↑, it is noteworthy that RA− represents strong chelating ability towards both Fe(ii) and Fe(iii) ions compared to its neutral form RA

2201- SK,    Shikonin promotes ferroptosis in HaCaT cells through Nrf2 and alleviates imiquimod-induced psoriasis in mice
- in-vitro, PSA, HaCaT - in-vivo, NA, NA
*eff↑, SHK treatment significantly improved imiquimod (IMQ)-induced psoriasis symptoms in mice
*IL6↓, attenuated the production of inflammatory cytokines, including interleukin (IL)-6, IL-17, and tumor necrosis factor-alpha (i.e., TNF-α)
*IL17↓,
*TNF-α↓,
*lipid-P↑, enhancing intracellular and mitochondrial ferrous and lipid peroxidation levels
*NRF2↓, by regulating expression of nuclear factor erythroid 2-related factor 2 (Nrf2), heme oxygenase-1 (HO-1), nuclear receptor coactivator 4 (NCOA4) and glutathione peroxidase 4 (GPX4)
*HO-1↝,
*NCOA4↝,
*GPx4↓, low dose SHK on LPS inhibited GPX4 and Nrf2 expression
*Ferroptosis↓, inhibited ferroptosis in psoriatic skin by reducing inflammation, ameliorating oxidative stress and iron accumulation.
*Inflam↓,
*ROS↓,
*Iron↓,


Showing Research Papers: 1 to 13 of 13

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 13

Pathway results for Effect on Cancer / Diseased Cells:


Redox & Oxidative Stress ⓘ

antiOx↑, 1,   Fenton↑, 2,   Ferroptosis↑, 2,   GPx4↓, 1,   Iron↓, 3,   i-Iron↓, 1,   lipid-P↑, 1,   NRF2↓, 2,   NRF2↑, 1,   ROS↑, 9,  

Metal & Cofactor Biology ⓘ

TfR1/CD71↓, 1,  

Core Metabolism/Glycolysis ⓘ

AMPK↑, 1,   GlucoseCon↓, 1,   lactateProd↓, 1,   LDHA↓, 1,   PKM2↓, 1,   SLC1A5↓, 1,   Warburg↓, 1,  

Cell Death ⓘ

Akt↓, 1,   Apoptosis↓, 1,   Apoptosis↑, 1,   BAX↑, 1,   Bcl-2↓, 1,   DR5↑, 1,   Ferroptosis↑, 2,  

Protein Folding & ER Stress ⓘ

ER Stress↑, 1,  

Autophagy & Lysosomes ⓘ

TumAuto↑, 1,  

Cell Cycle & Senescence ⓘ

TumCCA↑, 2,  

Proliferation, Differentiation & Cell State ⓘ

Gli1↓, 1,   HDAC2↓, 1,   mTOR↑, 1,   P70S6K↑, 1,   p‑PI3K↑, 1,  

Migration ⓘ

E-cadherin↑, 1,   MARK4↓, 1,   miR-155↓, 1,   MMP2↓, 1,   MMP9↓, 2,   N-cadherin↓, 1,   Vim↓, 1,  

Angiogenesis & Vasculature ⓘ

Hif1a↓, 1,  

Barriers & Transport ⓘ

GLUT1↓, 1,  

Drug Metabolism & Resistance ⓘ

ChemoSen↑, 2,   eff↑, 4,   selectivity↑, 1,  

Functional Outcomes ⓘ

AntiCan↑, 1,   chemoP↑, 1,  
Total Targets: 47

Pathway results for Effect on Normal Cells:


Redox & Oxidative Stress ⓘ

antiOx↑, 2,   Bil↓, 1,   Catalase↑, 2,   Copper↓, 2,   Fenton↓, 1,   Ferroptosis↓, 1,   GPx↑, 4,   GPx4↓, 1,   GSH↑, 3,   GSR↑, 1,   HDL↓, 1,   HO-1↓, 1,   HO-1↝, 1,   Iron↓, 9,   lipid-P↑, 1,   MDA↓, 3,   NRF2↓, 1,   NRF2↑, 1,   ROS↓, 8,   SOD↓, 1,   SOD↑, 3,  

Metal & Cofactor Biology ⓘ

FTL↓, 1,   IronCh↑, 2,   NCOA4↝, 1,   TfR1/CD71↓, 2,  

Core Metabolism/Glycolysis ⓘ

CREB↑, 1,   NADPH↓, 1,  

Cell Death ⓘ

Bax:Bcl2↓, 1,   Casp3↓, 1,   Casp3↑, 1,   Ferroptosis↓, 1,   iNOS↓, 1,  

Transcription & Epigenetics ⓘ

other↓, 1,  

Proliferation, Differentiation & Cell State ⓘ

ERK↑, 1,  

Migration ⓘ

Ca+2↝, 1,   PKA↑, 1,   PKCδ?, 1,  

Angiogenesis & Vasculature ⓘ

Hif1a↓, 1,   NO↓, 1,  

Barriers & Transport ⓘ

BBB↑, 2,  

Immune & Inflammatory Signaling ⓘ

IL17↓, 1,   IL1β↓, 1,   IL6↓, 1,   Inflam↓, 2,   TNF-α↓, 1,  

Cellular Microenvironment ⓘ

NOX↓, 1,  

Synaptic & Neurotransmission ⓘ

BDNF↑, 2,   PSD95↑, 2,  

Drug Metabolism & Resistance ⓘ

BioAv↝, 1,   Dose↝, 1,   eff↑, 1,  

Clinical Biomarkers ⓘ

Bil↓, 1,   IL6↓, 1,  

Functional Outcomes ⓘ

CardioT↓, 1,   cognitive↑, 2,   motorD↑, 1,   neuroP↑, 3,   RenoP↑, 1,   toxicity↓, 1,   toxicity∅, 1,  
Total Targets: 60

Scientific Paper Hit Count for: Iron, Iron
2 Artemisinin
2 Huperzine A/Huperzia serrata
2 Quercetin
2 Rosmarinic acid
1 Alpha-Lipoic-Acid
1 Carvacrol
1 HydroxyCitric Acid
1 Melatonin
1 Shikonin
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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