Psoralidin / Ki-67 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


Ki-67, Ki-67 protein: Click to Expand ⟱
Source:
Type: proliferation marker
A high Ki-67 proliferation index means many cells are dividing quickly and that the cancer is likely to grow and spread.
Markers of proliferation index (Ki-67)

• Ki-67 serves primarily as a proliferation marker: higher levels are generally indicative of aggressive disease and poorer outcomes across many cancer types.
• While Ki-67 itself is not considered a driver of tumorigenesis, its expression mirrors the high proliferative activity associated with protumoral behavior.
• It is widely used in clinical practice to aid in tumor grading, prognostication, and treatment planning.
Scientific Papers found: Click to Expand⟱
4968- PSO,    Psoralidin: emerging biological activities of therapeutic benefits and its potential utility in cervical cancer
- in-vitro, Cerv, NA
*Inflam↓, *antiOx↑, *neuroP↑, *AntiDiabetic↑, *Bacteria↓, AntiTum↑, CSCs↓, ROS↑, TumAuto↑, Apoptosis↑, ChemoSen↑, RadioS↑, BioAv↓, *cardioP↑, *ROS↓, *LDH↓, TumCP↓, TRAIL⇅, TumCMig↓, EMT↓, NF-kB↓, P53↑, Casp3↑, NOTCH↓, CSCs↓, angioG↓, VEGF↓, Ki-67↓, CD31↓, TRAILR↑, MMP↓, BioAv↓, BioAv↑,

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 ⓘ

ROS↑, 1,  

Mitochondria & Bioenergetics ⓘ

MMP↓, 1,  

Cell Death ⓘ

Apoptosis↑, 1,   Casp3↑, 1,   TRAIL⇅, 1,   TRAILR↑, 1,  

Autophagy & Lysosomes ⓘ

TumAuto↑, 1,  

DNA Damage & Repair ⓘ

P53↑, 1,  

Proliferation, Differentiation & Cell State ⓘ

CSCs↓, 2,   EMT↓, 1,   NOTCH↓, 1,  

Migration ⓘ

CD31↓, 1,   Ki-67↓, 1,   TumCMig↓, 1,   TumCP↓, 1,  

Angiogenesis & Vasculature ⓘ

angioG↓, 1,   VEGF↓, 1,  

Immune & Inflammatory Signaling ⓘ

NF-kB↓, 1,  

Drug Metabolism & Resistance ⓘ

BioAv↓, 2,   BioAv↑, 1,   ChemoSen↑, 1,   RadioS↑, 1,  

Clinical Biomarkers ⓘ

Ki-67↓, 1,  

Functional Outcomes ⓘ

AntiTum↑, 1,  
Total Targets: 24

Pathway results for Effect on Normal Cells:


Redox & Oxidative Stress ⓘ

antiOx↑, 1,   ROS↓, 1,  

Core Metabolism/Glycolysis ⓘ

LDH↓, 1,  

Immune & Inflammatory Signaling ⓘ

Inflam↓, 1,  

Clinical Biomarkers ⓘ

LDH↓, 1,  

Functional Outcomes ⓘ

AntiDiabetic↑, 1,   cardioP↑, 1,   neuroP↑, 1,  

Infection & Microbiome ⓘ

Bacteria↓, 1,  
Total Targets: 9

Scientific Paper Hit Count for: Ki-67, Ki-67 protein
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#:425  State#:%  Dir#:%
  wNotes=0  sortOrder:rid,rpid

 

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