Psoralidin / GPx4 Cancer Research Results

PSO, Psoralidin: Click to Expand ⟱
Features:
Psoralidin is a prenylated coumestan isolated primarily from Psoralea corylifolia (Babchi). It is not a classical anticancer drug.
Psoralidin generally acts to suppress oncogenic signaling and survival pathways while promoting apoptosis in tumor cells.
Reported effects (context-dependent, preclinical):
-DOWNREGULATES pro-survival pathways (e.g., NF-κB, STAT3)
-UPREGULATES apoptotic signaling (caspase activation)
-MODULATES androgen receptor signaling in prostate cancer models
-SENSITIZES tumor cells to chemo- and radio-induced stress

This positions psoralidin as a biologic modulator, not a driver.

Across cancer cell and animal models, psoralidin has been associated with:
-Apoptosis induction
  -Caspase activation
  -Mitochondrial depolarization
-Inflammatory pathway suppression
  -NF-κB inhibition
  -STAT3 attenuation
-Hormone signaling modulation
  -Androgen receptor suppression (prostate cancer context)
-Oxidative stress interaction
  -Redox imbalance tipping tumor cells toward death under stress

Psoralidin is best described as chemopreventive or chemo-sensitizing, not chemoprotective


GPx4, Glutathione Peroxidase 4: Click to Expand ⟱
Source:
Type:
GPX4 (Glutathione Peroxidase 4) is a selenoprotein that plays a crucial role in the regulation of ferroptosis, a form of programmed cell death characterized by the iron-dependent accumulation of lipid reactive oxygen species (ROS).
GPX4 has been found to be upregulated in several tumor types, promoting cancer cell survival and resistance to therapy. For instance, GPX4 overexpression has been observed in renal cell carcinoma, pancreatic ductal adenocarcinoma, and triple-negative breast cancer, among others. -GPX4 is known as a lipid peroxidation inhibitor protein, and its antioxidant effect is closely related to ferrous iron
Scientific Papers found: Click to Expand⟱
4965- PSO,  Cisplatin,    The synergistic antitumor effects of psoralidin and cisplatin in gastric cancer by inducing ACSL4-mediated ferroptosis
- vitro+vivo, GC, HGC27 - vitro+vivo, GC, MKN45
TumCP↓, TumCMig↓, TumCI↓, TumCG↓, *toxicity↓, eff↑, Ferroptosis↑, ACSL4↑, GPx4↓, ChemoSen↑, chemoP↑, AntiTum↑, Sepsis↓,

Showing Research Papers: 1 to 1 of 1

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 1

Pathway results for Effect on Cancer / Diseased Cells:


Redox & Oxidative Stress ⓘ

Ferroptosis↑, 1,   GPx4↓, 1,  

Core Metabolism/Glycolysis ⓘ

ACSL4↑, 1,  

Cell Death ⓘ

Ferroptosis↑, 1,  

Proliferation, Differentiation & Cell State ⓘ

TumCG↓, 1,  

Migration ⓘ

TumCI↓, 1,   TumCMig↓, 1,   TumCP↓, 1,  

Drug Metabolism & Resistance ⓘ

ChemoSen↑, 1,   eff↑, 1,  

Functional Outcomes ⓘ

AntiTum↑, 1,   chemoP↑, 1,  

Infection & Microbiome ⓘ

Sepsis↓, 1,  
Total Targets: 13

Pathway results for Effect on Normal Cells:


Functional Outcomes ⓘ

toxicity↓, 1,  
Total Targets: 1

Scientific Paper Hit Count for: GPx4, Glutathione Peroxidase 4
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:%  Cells:%  prod#:389  Target#:643  State#:%  Dir#:%
  wNotes=0  sortOrder:rid,rpid

 

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