VitK3,menadione / E-cadherin Cancer Research Results

VitK3, VitK3,menadione: Click to Expand ⟱
Features:
Menadione (2-methyl-1,4-naphthoquinone, also termed vitamin K3)
Menadione-induced ROS generation is concentration-dependent and high concentrations trigger cell death.
Clinical trials conducted on patients with prostate cancer showed that ascorbic acid-menadione produced an immediate drop in tumor cell numbers through a mechanism named autoschizis.
Menadione (Vitamin K3) is a synthetic naphthoquinone compound. It is not used as a nutritional vitamin supplement in humans due to toxicity risk (particularly hemolysis and hepatotoxicity). Historically used in animal feed.
Mechanistically, menadione functions primarily as a redox-active quinone, capable of:
-Undergoing redox cycling
-Generating reactive oxygen species (ROS)
-Inducing oxidative stress
-Interacting with glutathione (GSH) systems
-Modulating mitochondrial function
It has been investigated in oncology research largely due to its pro-oxidant cytotoxic properties, not classical vitamin K–dependent clotting roles.

Rank Pathway / Axis Cancer / Tumor Context Normal Tissue Context TSF Primary Effect Notes / Interpretation
1 Redox cycling (quinone-mediated ROS generation) ROS ↑; oxidative stress ↑; apoptosis ↑ (dose-dependent) Oxidative injury risk ↑ (hemolysis, hepatotoxicity) P, R Primary cytotoxic mechanism Menadione undergoes one-electron redox cycling, generating superoxide and hydrogen peroxide; not selective for tumor cells.
2 Glutathione (GSH) depletion GSH ↓; redox buffering capacity ↓ Red cell vulnerability ↑ P, R Redox destabilization Conjugation and oxidative cycling consume GSH, amplifying oxidative stress.
3 Mitochondrial dysfunction ΔΨm ↓; ATP ↓; apoptosis signaling ↑ Energy stress in normal cells possible R, G Mitochondria-mediated apoptosis ROS and redox imbalance disrupt mitochondrial membrane potential.
4 DNA damage (oxidative) DNA strand breaks ↑ (reported) Genotoxic risk ↑ R, G Genome instability Often secondary to ROS accumulation rather than direct DNA intercalation.
5 Synergy with ascorbate (Vitamin C) Redox cycling ↑; cytotoxicity ↑ (reported in vitro) Systemic oxidative injury risk ↑ P, R Redox amplification Menadione can undergo redox cycling with ascorbate, increasing ROS production; largely preclinical data.
6 Topoisomerase interference (reported) Topo inhibition (context-dependent) ↔ R Secondary mechanism Some studies report interference with topoisomerase activity, but this is not the dominant mechanism.
7 Hemolysis risk (G6PD vulnerability) — Red blood cell destruction risk ↑ R Major toxicity constraint Menadione can cause hemolytic anemia, especially in G6PD deficiency.
8 Hepatotoxicity — Liver injury risk ↑ G Clinical toxicity constraint Historical reason for discontinuation as a human supplement.
9 Vitamin K–dependent clotting pathway Minimal physiologic role in humans Not equivalent to K1/K2 — Classification clarification Menadione is a synthetic precursor; does not function identically to phylloquinone (K1) or menaquinones (K2).

Time-Scale Flag (TSF): P / R / G

  • P: 0–30 min (rapid redox cycling and ROS generation)
  • R: 30 min–3 hr (mitochondrial dysfunction, DNA damage signaling)
  • G: >3 hr (apoptosis, tissue-level toxicity outcomes)
E-cadherin, E-cadherin: Click to Expand ⟱
Source: HalifaxProj(restore)
Type:
Also known as Cadherin1 (CDH1)
E-cadherin, is a type of cell adhesion molecule that plays a crucial role in maintaining tissue structure and cell-cell interactions. In the context of cancer, E-cadherin has been found to be a tumor suppressor gene.

E-cadherin is a transmembrane protein that mediates cell-cell adhesion through its extracellular domain, which interacts with other E-cadherin molecules on adjacent cells. This interaction helps to maintain tissue integrity and prevent cancer cells from invading surrounding tissues.

In many types of cancer, including breast, colon, and prostate cancer, E-cadherin expression is often reduced or lost.
cell adhesion molecules spanning four families of 1) Integrins (α2β1, α5/β1, αL/β2); 2) Cadherins (E-cad, P-cad, N-cad); 3) Ig-CAMs (VCAM, NCAM, ICAM, Nectins, Necl); and 4) Selectins (E-selectin, P-selectin, L-selectin).
Scientific Papers found: Click to Expand⟱
1821- VitK3,    Menadione (Vitamin K3) induces apoptosis of human oral cancer cells and reduces their metastatic potential by modulating the expression of epithelial to mesenchymal transition markers and inhibiting migration
- in-vitro, Oral, NA - in-vitro, Nor, HEK293 - in-vitro, Nor, HaCaT
selectivity↑, TumCD↓, BAX↑, P53↑, Bcl-2↓, p65↓, E-cadherin↑, EMT↓, Vim↓, Fibronectin↓, TumCG↓, TumCMig↓,
1820- VitK3,    Vitamin K3 (menadione) suppresses epithelial-mesenchymal-transition and Wnt signaling pathway in human colorectal cancer cells
- in-vitro, CRC, SW480 - in-vitro, CRC, SW-620
selectivity↑, TumCI↓, TumCMig↓, EMT↓, E-cadherin↑, ZO-1↑, N-cadherin↓, Vim↓, Zeb1↓, MMP2↓, MMP9↓, TOPflash↓, β-catenin/ZEB1↓, p300↓, cycD1/CCND1↓, TumCCA↑,

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:


Cell Death ⓘ

BAX↑, 1,   Bcl-2↓, 1,   TumCD↓, 1,  

DNA Damage & Repair ⓘ

P53↑, 1,  

Cell Cycle & Senescence ⓘ

cycD1/CCND1↓, 1,   TumCCA↑, 1,  

Proliferation, Differentiation & Cell State ⓘ

EMT↓, 2,   p300↓, 1,   TOPflash↓, 1,   TumCG↓, 1,  

Migration ⓘ

E-cadherin↑, 2,   Fibronectin↓, 1,   MMP2↓, 1,   MMP9↓, 1,   N-cadherin↓, 1,   TumCI↓, 1,   TumCMig↓, 2,   Vim↓, 2,   Zeb1↓, 1,   ZO-1↑, 1,   β-catenin/ZEB1↓, 1,  

Immune & Inflammatory Signaling ⓘ

p65↓, 1,  

Drug Metabolism & Resistance ⓘ

selectivity↑, 2,  
Total Targets: 23

Pathway results for Effect on Normal Cells:


Total Targets: 0

Scientific Paper Hit Count for: E-cadherin, E-cadherin
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#:230  Target#:89  State#:%  Dir#:2
  wNotes=0  sortOrder:rid,rpid

 

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