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.
Pca, Prostate Cancer: Click to Expand ⟱
Prostate Cancer: Alterations in genes such as ERG, SPOP, MYC, androgen receptor (AR), and CHD1, drive PCa progression.
TP53 is the most commonly mutated gene in human cancer.
HH↑, GLI-1↑, SHH↑ P53↓
The loss of p53 and/or other tumor suppressor genes, reduced capacity for DNA repair, the dysfunction of telomerase activity, and changes in the pathways that govern the growth of cells also mediate the progression of Pca.
It has been well documented that Ca2+ influx and MDR1 upregulation are highly associated with GEM metabolism in human pancreatic carcinoma.
Increased Growth factor IGF-1/IGF-1R axis activation mediated by both PI3K/Akt or RAF/MEK/ERK system and AR expression remains important in the development and progression of prostate cancer.
It has been demonstrated that prostate cancer cells are relatively sensitive to heat stress.
Long non-coding RNA MALAT1 has been reported as an oncogenic target in multiple types of cancers, including PC.
Scientific Papers found: Click to Expand⟱
582- MF,  immuno,  VitC,    Magnetic field boosted ferroptosis-like cell death and responsive MRI using hybrid vesicles for cancer immunotherapy
- in-vitro, Pca, TRAMP-C1 - in-vivo, NA, NA
Fenton↑, Ferroptosis↑, ROS↑, TumCG↓, Iron↑, GPx4↓,
4892- Sper,  erastin,    Spermidine inactivates proteasome activity and enhances ferroptosis in prostate cancer
- in-vitro, Pca, PC3 - in-vivo, Pca, NA
Ferroptosis↑, lipid-P↑, Iron↑, eff↑, HO-1↑, NRF2↑, ROS↑, AntiTum↑, eff↓,
5091- SSE,    Superoxide-mediated ferroptosis in human cancer cells induced by sodium selenite
- in-vitro, GBM, U87MG - in-vitro, Cerv, HeLa - in-vitro, BC, MCF-7 - in-vitro, Pca, PC3 - in-vitro, CRC, HT-29 - in-vitro, Nor, SVGp12
Ferroptosis↑, xCT↓, GSH↓, GPx4↓, Iron↑, lipid-P↑, ROS↑, eff↓, TumCP↓, TumCD↑,
5088- SSE,    Superoxide-mediated ferroptosis in human cancer cells induced by sodium selenite
- in-vitro, BC, MCF-7 - in-vitro, GBM, U87MG - in-vitro, Pca, PC3 - in-vitro, Cerv, HeLa - in-vitro, GBM, A172
Ferroptosis↑, ROS↑, Iron↑, xCT↓, GSH↓, GPx4↓, lipid-P↑, TumCP↓, selectivity↑,

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↑, 1,   Ferroptosis↑, 4,   GPx4↓, 3,   GSH↓, 2,   HO-1↑, 1,   Iron↑, 4,   lipid-P↑, 3,   NRF2↑, 1,   ROS↑, 4,   xCT↓, 2,  

Cell Death ⓘ

Ferroptosis↑, 4,   TumCD↑, 1,  

Proliferation, Differentiation & Cell State ⓘ

TumCG↓, 1,  

Migration ⓘ

TumCP↓, 2,  

Drug Metabolism & Resistance ⓘ

eff↓, 2,   eff↑, 1,   selectivity↑, 1,  

Functional Outcomes ⓘ

AntiTum↑, 1,  
Total Targets: 18

Pathway results for Effect on Normal Cells:


Total Targets: 0

Scientific Paper Hit Count for: Iron, Iron
2 Selenite (Sodium)
1 Magnetic Fields
1 immunotherapy
1 Vitamin C (Ascorbic Acid)
1 Spermidine
1 erastin
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

Filter Conditions: Pro/AntiFlg:%  IllCat:%  CanType:22  Cells:%  prod#:%  Target#:160  State#:%  Dir#:2
  wNotes=0  sortOrder:rid,rpid

 

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