Ferritin Cancer Research Results

Ferritin, SF serum Ferritin: Click to Expand ⟱
Source:
Type:
It is widely accepted that there is a strong relationship between iron levels and cancer. . Serum ferritin levels are elevated in many malignancies.
Gynecological malignant tumor patients with high serum ferritin levels have significantly less survival time than patients with low or normal serum ferritin levels.
Ferritin is the primary intracellular iron-storage protein, with small amounts released into circulation. Biologically, ferritin buffers iron to prevent oxidative damage. Clinically, serum ferritin is a composite signal reflecting iron stores and inflammation.

Key point: In cancer, ferritin behaves more like an inflammatory biomarker than a pure iron marker.

In oncology, high ferritin usually reflects one or more of the following:
-IL-6–driven inflammation (acute-phase response)
-Iron sequestration (functional iron deficiency despite high ferritin)
-Tumor-associated macrophage activity
-Cell death and tissue breakdown
-Liver involvement (secondary contributor)

Thus, ferritin integrates immune activation + metabolic stress.


Scientific Papers found: Click to Expand⟱
2756- BetA,    Betulinic acid inhibits growth of hepatoma cells through activating the NCOA4-mediated ferritinophagy pathway
- in-vitro, HCC, HUH7 - in-vitro, HCC, H1299
TumCP↓, betulinic acid could suppress proliferation and migration of hepatoma cells, raised ROS level and inhibited antioxidation level in cells
ROS↑,
antiOx↓,
TumCG↓, These findings indicate that betulinic acid has the capacity to significantly impede hepatoma cells growth and migration
TumCMig↓,
NRF2↓, The expression of antioxidant proteins Nrf2, GPX4 and HO-1 was also considerably lower in the BETM and BETH groups than in the Control group
GPx4↓,
HO-1↓,
NCOA4↑, suggesting that betulinic acid activates ferritinophagy by boosting NCOA4 expression and FTH1 degradation.
FTH1↓, betulinic acid groups (10 mg/kg, 20 mg/kg, and 40 mg/kg) greatly boosted LC3II and NCOA4 expressions and suppressed FTH1
Ferritin↑, In summation, betulinic acid decreases antioxidation in tumour tissues from nude mice, inhibits ferritin expression, enhances the expression of ferritinophagy-associated protein, activates ferritinophagy, and initiates ferroptosis in tumour cells.
Ferroptosis↑,
GSH↓, In comparison to the Control group, the betulinic acid groups (10 mg/kg, 20 mg/kg and 40 mg/kg) reduced dramatically GSH and hydroxyl radical inhibition capacity in serum, considerably increased serum Fe2+), and decreased dramatically serum MDA
MDA↓,

3576- CUR,    Protective Effects of Indian Spice Curcumin Against Amyloid-β in Alzheimer's Disease
- Review, AD, NA
*Inflam↓, known to have protective effects, including anti-inflammatory, antioxidant, anti-arthritis, pro-healing, and boosting memory cognitive functions.
*antiOx↑,
*memory↑,
*Aβ↓, curcumin prevents Aβ aggregation and crosses the blood-brain barrier,
*BBB↑,
*cognitive↑, curcumin ameliorates cognitive decline and improves synaptic functions in mouse models of AD
*tau↓, curcumin's effect on inhibition of A and tau,copper binding ability, cholesterol lowering ability, anti-inflammatory and modulation of microglia, acetylcholinesterase (AChE) inhibition, antioxidant properties,
*LDL↓,
*AChE↓,
*IL1β↓, Curcumin reduced the levels of oxidized proteins and IL1B in the brains of APP mice
*IronCh↑, Curcumin binds to redox-active metals, iron and copper
*neuroP↑, Curcumin, a neuroprotective agent, has poor brain bioavailability.
*BioAv↝,
*PI3K↑, They found that curcumin significantly upregulates phosphatidylinositol 3-kinase (PI3K), Akt, nuclear factor E2-related factor-2 (Nrf2), heme oxygenase 1, and ferritin expression
*Akt↑,
*NRF2↑,
*HO-1↑,
*Ferritin↑,
*HO-2↓, and that it significantly downregulates heme oxygenase 2, ROS, and A40/42 expression.
*ROS↓,
*Ach↑, significant increase in brain ACh, glutathione, paraoxenase, and BCL2 levels with respect to untreated group associated with significant decrease in brain AChE activity,
*GSH↑,
*Bcl-2↑,
*ChAT↑, nvestigation revealed that the selected treatments caused marked increase in ChAT positive cells.


Showing Research Papers: 1 to 2 of 2

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 2

Pathway results for Effect on Cancer / Diseased Cells:


Redox & Oxidative Stress ⓘ

antiOx↓, 1,   Ferroptosis↑, 1,   GPx4↓, 1,   GSH↓, 1,   HO-1↓, 1,   MDA↓, 1,   NRF2↓, 1,   ROS↑, 1,  

Metal & Cofactor Biology ⓘ

Ferritin↑, 1,   FTH1↓, 1,   NCOA4↑, 1,  

Cell Death ⓘ

Ferroptosis↑, 1,  

Proliferation, Differentiation & Cell State ⓘ

TumCG↓, 1,  

Migration ⓘ

TumCMig↓, 1,   TumCP↓, 1,  

Clinical Biomarkers ⓘ

Ferritin↑, 1,  
Total Targets: 16

Pathway results for Effect on Normal Cells:


Redox & Oxidative Stress ⓘ

antiOx↑, 1,   GSH↑, 1,   HO-1↑, 1,   HO-2↓, 1,   NRF2↑, 1,   ROS↓, 1,  

Metal & Cofactor Biology ⓘ

Ferritin↑, 1,   IronCh↑, 1,  

Core Metabolism/Glycolysis ⓘ

LDL↓, 1,  

Cell Death ⓘ

Akt↑, 1,   Bcl-2↑, 1,  

Transcription & Epigenetics ⓘ

Ach↑, 1,  

Proliferation, Differentiation & Cell State ⓘ

PI3K↑, 1,  

Barriers & Transport ⓘ

BBB↑, 1,  

Immune & Inflammatory Signaling ⓘ

IL1β↓, 1,   Inflam↓, 1,  

Synaptic & Neurotransmission ⓘ

AChE↓, 1,   ChAT↑, 1,   tau↓, 1,  

Protein Aggregation ⓘ

Aβ↓, 1,  

Drug Metabolism & Resistance ⓘ

BioAv↝, 1,  

Clinical Biomarkers ⓘ

Ferritin↑, 1,  

Functional Outcomes ⓘ

cognitive↑, 1,   memory↑, 1,   neuroP↑, 1,  
Total Targets: 25

Scientific Paper Hit Count for: Ferritin, SF serum Ferritin
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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