Iron Cancer Research Results

Iron, Iron: Click to Expand ⟱
Source:
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⟱
568- ART/DHA,    Mechanism-Guided Design and Synthesis of a Mitochondria-Targeting Artemisinin Analogue with Enhanced Anticancer Activity
- in-vitro, NA, MDA-MB-231 - in-vitro, NA, HeLa - in-vitro, NA, SkBr3 - in-vitro, NA, HCT116
Iron↝, free heme is the main activator

8135- LF,    Lactoferrin-A Regulator of Iron Homeostasis and Its Implications in Cancer
- Review, Var, NA - Review, AD, NA
IronCh↑, Lactoferrin (LF), a glycoprotein with strong iron chelating properties, can regulate its availability to cancer cells, thereby limiting their growth and progression.
ROS↓, By chelating free Fe ions, LF reduces oxidative stress and inhibits the mechanisms that promote carcinogenesis.
Imm↑, Additionally, it exhibits immunomodulatory and anti-inflammatory effects and may enhance the body’s anti-tumor response.
Inflam↓,
*BBB↑, LF crosses from the blood into the cerebrospinal fluid through the blood–brain barrier [25], where its beneficial effects have been documented in the context of neurodegenerative diseases such as Parkinson’s disease, Alzheimer’s disease, and de
Iron↝, Among the many biological properties of lactoferrin, its ability to strongly bind and transport iron ions over a wide range of pH values is a key function, determining its effectiveness in regulating iron homeostasis
*Fenton↓, LF, due to its ability to chelate iron, reduces its availability for the Fenton reaction, which reduces oxidative stress
*ROS↓,
*TAC↑, antioxidant properties of LF supplementation resulted in an increase in hydrophilic antioxidant capacity [151], a decrease in oxidative stress markers [152,153], and an increase in total antioxidant status (TAS)
*SOD↑, It also improved the levels of antioxidant markers, such as SOD, GPx, and glutathione, compared with the placebo group
*GPx↑,
*GSH↑,
*TBARS↓, Supplementation with LF-containing colostrum led to lower levels of thiobarbituric acid reactive substances (TBARS).
*PTEN↓, In addition, in patients with Alzheimer’s disease, LF supplementation led to the decreased expression of phosphatase and tensin homolog (PTEN), tau, and mitogen-activated protein kinase (MAPK1), as well as decreased serum levels of Aβ42, which ma
*tau↓,
*MAPK↓,
*Aβ42↓,
*Apoptosis↓, Reducing hydrogen peroxide-induced apoptosis through the inhibition of caspase-3 and Akt activation
*Casp3↓,
*Akt↑,
*GutMicro↑, LF shows a beneficial effect on the composition of the microbiota, promoting the growth of beneficial bacteria such as Bifidobacterium and Lactobacillus, while inhibiting the growth of pathogens such as Escherichia coli, Salmonella, and Shigella.
*Sepsis↓, A meta-analysis suggests that it may reduce the risk of fungal sepsis and shorten the hospitalization of preterm infants
*anemia↓, LF administration is a promising therapy for iron deficiency (ID) conditions, including iron deficiency anemia (IDA), both as a primary treatment and as an adjunctive therapy.
*IL6↓, ability to inhibit interleukin-6 (IL-6) expression, LF decreases hepcidin synthesis, which in turn increases ferroportin levels, restoring iron export from cells to the blood i
*FPN↑,
*TfR1/CD71↑, In addition, LF induces an increase in transferrin receptor 1 (TfR1) levels and a decrease in ferritin (Ftn) levels
*Ferritin↓,
*HemoG↑, Numerous intervention studies have confirmed the efficacy of LF supplementation, showing an increase in hemoglobin (Hb), total iron, erythrocyte count (RBC), and serum ferritin levels.
*RBC↑,
*eff↑, Most studies have shown similar or superior efficacy of bLF to traditionally used therapy (ferrous sulfate and ferric hydroxide) in restoring iron deficiency, with significantly fewer gastrointestinal side effects
*BioAv↓, Orally administered LF has low bioavailability due to degradation at unfavorable gastric pH and by proteolytic enzymes in the intestinal lumen and poor permeability through the intestinal epithelium, which limits its effective delivery to target site
*BioAv↑, LF is much better absorbed when administered directly into the duodenum. Therefore, ... coating enteral capsules containing LF, encapsulating it in nanocarriers, which allows it to be released at a site with less gastric pepsin activity
*BioAv↝, Other routes of administration, including transdermal or inhalation, are also being considered, which could avoid degradation in the gastrointestinal tract.
*ChemoSen↑, studies suggest that LF may act synergistically with other therapies such as chemotherapy, immunotherapy, and targeted therapy
*BioAv↑, Additionally, the use of probiotic bacteria as internal producers of LF in the body may open new perspectives for its therapeutic use.
Ferroptosis↑, LF also induces ferroptosis—iron-dependent cell death, which leads to excessive lipid oxidation in cell membranes and the destruction of cancer cells.

8139- LF,    Androgen Receptor‐Induced Lactoferrin Accelerates Prostate Tumorigenesis Through Modulating Ferroptosis
- vitro+vivo, Pca, NA
Ferroptosis↓, Mechanistically, lactoferrin shields prostate cancer cells from iron‐induced ferroptosis by maintaining iron‐redox homeostasis.
AR↝, This work defines lactoferrin as: (i) an AR‐regulated ferroptosis suppressor,
Iron↝, (ii) a regulator of prostate cancer's “iron addiction,” and (iii) a candidate target for therapeutic exploitation of iron‐metabolic vulnerability.
Ferritin↑, This study demonstrates that transcription factor androgen receptor (AR) directly binds the LF promoter, driving lactoferrin overexpression to promote ferritin (FTH1/FTL) upregulation and inhibit p53‐ALOX12‐mediated ferroptosis in prostate cancer
P53↓,
eff↝, Lactoferrin Deficiency Delays Prostate Tumorigenesis in TRAMP Mice
other↝, The current study revealed that lactoferrin is a previously unrecognized oncogene in prostate cancer, elucidating a novel AR‐lactoferrin‐ferroptosis regulatory axis with potential therapeutic prospects.
AntiTum↓, Contrary to its established tumor‐suppressive functions, we find that in prostate cancer, lactoferrin can exhibit oncogenic properties, a function that is mechanistically linked to and dependent on AR signaling.

7825- LT,  MBS,    Neuroprotective Potential of Mung Bean (Vigna radiata L.) Polyphenols in Alzheimer's Disease: A Review
- Review, AD, NA
*neuroP↑, neuroprotective activity of luteolin was also observed in a transgenic Drosophila model.
*OS↑, showed that luteolin extend the life span of Drosophila, enhanced its antioxidative ability, and directly bound to Aβ42 and AChE to inhibit the Aβ aggregation and cholinergic deficits
*antiOx↑,
*Aβ42↓,
*AChE↓,
*Aβ↓,
*IRes↓, It was found that luteolin (50 mg/kg) reduced cerebral insulin resistance and tau hyperphosphorylation in a high fat diet (HFD
*p‑tau↓,
*ROS↓, neuroprotective activity in AD was achieved by inhibition of oxidative stress, apoptosis, neuroinflammation, AChE activity, cerebral insulin resistance, or iron imbalance.
*Apoptosis↓,
*Inflam↓,
*Iron↝,

1216- VitC,    Ascorbic acid induces ferroptosis via STAT3/GPX4 signaling in oropharyngeal cancer
- in-vitro, Laryn, FaDu - in-vitro, SCC, SCC-154
Iron↝, impairing iron metabolism
ROS↑,
tumCV↓,
Ki-67↓,
TumCCA↑, accumulation in the G0/G1 phase
Ferroptosis↑,
GSH↓,
ROS↑,
MDA↑,
STAT3↓,
GPx4↓,
p‑STAT3↓,


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(tgid=1) ⓘ

Ferroptosis↓, 1,   Ferroptosis↑, 2,   GPx4↓, 1,   GSH↓, 1,   Iron↝, 4,   MDA↑, 1,   ROS↓, 1,   ROS↑, 2,  

Metal & Cofactor Biology(tgid=2) ⓘ

Ferritin↑, 1,   IronCh↑, 1,  

Cell Death(tgid=5) ⓘ

Ferroptosis↓, 1,   Ferroptosis↑, 2,  

Transcription & Epigenetics(tgid=7) ⓘ

other↝, 1,   tumCV↓, 1,  

DNA Damage & Repair(tgid=10) ⓘ

P53↓, 1,  

Cell Cycle & Senescence(tgid=11) ⓘ

TumCCA↑, 1,  

Proliferation, Differentiation & Cell State(tgid=12) ⓘ

STAT3↓, 1,   p‑STAT3↓, 1,  

Migration(tgid=13) ⓘ

Ki-67↓, 1,  

Immune & Inflammatory Signaling(tgid=16) ⓘ

Imm↑, 1,   Inflam↓, 1,  

Hormonal & Nuclear Receptors(tgid=20) ⓘ

AR↝, 1,  

Drug Metabolism & Resistance(tgid=21) ⓘ

eff↝, 1,  

Clinical Biomarkers(tgid=22) ⓘ

AR↝, 1,   Ferritin↑, 1,   Ki-67↓, 1,  

Functional Outcomes(tgid=23) ⓘ

AntiTum↓, 1,  
Total Targets: 27

Pathway results for Effect on Normal Cells:


NA, unassigned(tgid=0) ⓘ

anemia↓, 1,   Aβ42↓, 2,   FPN↑, 1,   IRes↓, 1,   RBC↑, 1,  

Redox & Oxidative Stress(tgid=1) ⓘ

antiOx↑, 1,   Fenton↓, 1,   GPx↑, 1,   GSH↑, 1,   Iron↝, 1,   ROS↓, 2,   SOD↑, 1,   TAC↑, 1,   TBARS↓, 1,  

Metal & Cofactor Biology(tgid=2) ⓘ

Ferritin↓, 1,   TfR1/CD71↑, 1,  

Cell Death(tgid=5) ⓘ

Akt↑, 1,   Apoptosis↓, 2,   Casp3↓, 1,   MAPK↓, 1,  

Proliferation, Differentiation & Cell State(tgid=12) ⓘ

PTEN↓, 1,  

Barriers & Transport(tgid=15) ⓘ

BBB↑, 1,  

Immune & Inflammatory Signaling(tgid=16) ⓘ

IL6↓, 1,   Inflam↓, 1,  

Synaptic & Neurotransmission(tgid=18) ⓘ

AChE↓, 1,   tau↓, 1,   p‑tau↓, 1,  

Protein Aggregation(tgid=19) ⓘ

Aβ↓, 1,  

Drug Metabolism & Resistance(tgid=21) ⓘ

BioAv↓, 1,   BioAv↑, 2,   BioAv↝, 1,   ChemoSen↑, 1,   eff↑, 1,  

Clinical Biomarkers(tgid=22) ⓘ

Ferritin↓, 1,   GutMicro↑, 1,   HemoG↑, 1,   IL6↓, 1,  

Functional Outcomes(tgid=23) ⓘ

neuroP↑, 1,   OS↑, 1,  

Infection & Microbiome(tgid=24) ⓘ

Sepsis↓, 1,  
Total Targets: 40

Scientific Paper Hit Count for: Iron, Iron
2 Lactoferrin/Talactoferrin
1 Artemisinin
1 Luteolin
1 Mung Bean Sprouts
1 Vitamin C (Ascorbic Acid)
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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