VitK3,menadione / MMP9 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)
MMP9, MMP9: Click to Expand ⟱
Source: HalifaxProj(suppress)
Type:
Matrix metalloproteinase-9 (MMP-9) is an enzyme that plays a significant role in the degradation of extracellular matrix components.
MMP-9 facilitates the breakdown of the extracellular matrix, which can enable cancer cells to invade surrounding tissues and spread to distant sites (metastasis).
Elevated levels of MMP-9 have been associated with poor prognosis in several cancers, including breast, lung, and colorectal cancers.
MMP2 and MMP9: two enzymes are critical to tumor invasion.
Scientific Papers found: Click to Expand⟱
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 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 Cycle & Senescence ⓘ

cycD1/CCND1↓, 1,   TumCCA↑, 1,  

Proliferation, Differentiation & Cell State ⓘ

EMT↓, 1,   p300↓, 1,   TOPflash↓, 1,  

Migration ⓘ

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

Drug Metabolism & Resistance ⓘ

selectivity↑, 1,  
Total Targets: 16

Pathway results for Effect on Normal Cells:


Total Targets: 0

Scientific Paper Hit Count for: MMP9, MMP9
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#:203  State#:%  Dir#:1
  wNotes=0  sortOrder:rid,rpid

 

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