Psoralidin / FAK 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


FAK, FAK signaling: Click to Expand ⟱
Source: HalifaxProj(inhibit)
Type:
FAK (Focal Adhesion Kinase) is a non-receptor tyrosine kinase that plays a crucial role in cellular processes such as adhesion, migration, proliferation, and survival. It is primarily localized at focal adhesions, where it interacts with integrins and other signaling molecules. FAK promotes cell proliferation by activating signaling pathways such as the PI3K/Akt and MAPK/ERK pathways. These pathways are often upregulated in cancer cells, leading to uncontrolled growth.
Scientific Papers found: Click to Expand⟱
4967- PSO,    Psoralidin's Anti-Cancer Mechanisms: A Technical Guide
- Review, Var, NA
NF-kB↓, PI3K↓, Akt↓, ITGB1↓, FAK↓, BAX↑, Casp3↑, Apoptosis↑, Bcl-2↓, DR5↑, TumCCA↑, TumAuto↑, TumMeta↓,

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:


Cell Death ⓘ

Akt↓, 1,   Apoptosis↑, 1,   BAX↑, 1,   Bcl-2↓, 1,   Casp3↑, 1,   DR5↑, 1,  

Autophagy & Lysosomes ⓘ

TumAuto↑, 1,  

Cell Cycle & Senescence ⓘ

TumCCA↑, 1,  

Proliferation, Differentiation & Cell State ⓘ

PI3K↓, 1,  

Migration ⓘ

FAK↓, 1,   ITGB1↓, 1,   TumMeta↓, 1,  

Immune & Inflammatory Signaling ⓘ

NF-kB↓, 1,  
Total Targets: 13

Pathway results for Effect on Normal Cells:


Total Targets: 0

Scientific Paper Hit Count for: FAK, FAK signaling
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#:110  State#:%  Dir#:1
  wNotes=0  sortOrder:rid,rpid

 

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