VitK3,menadione / p65 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)
p65, RelA: Click to Expand ⟱
Source:
Type:
P65, also known as RelA, is a subunit of the NF-κB (nuclear factor kappa-light-chain-enhancer of activated B cells) transcription factor complex. NF-κB plays a crucial role in regulating immune response, inflammation, and cell survival.
Due to its role in cancer progression, p65 and the NF-κB pathway are considered potential therapeutic targets. Inhibitors of NF-κB signaling are being explored in preclinical and clinical studies as potential cancer treatments.
Many studies have reported that p65 is overexpressed in various types of cancers, including breast, prostate, lung, and colorectal cancers.
In some cancers, elevated p65 levels correlate with higher grades of tumors and advanced stages of disease.

"RELA proto-oncogene, NF-κB subunit." It encodes the p65 protein, which is a central component of the NF‑κB transcription factor complex.
-Chronic activation of RELA and the NF‑κB pathway is frequently associated with cancer progression, promoting inflammation-driven tumorigenesis, chemoresistance, and metastasis.
-RELA interacts with other oncogenic signaling networks (for example, STAT3 and MAPK pathways), further integrating environmental signals that favor cancer progression.

RELA (p65) is a critical subunit of the NF‑κB transcription factor complex, involved in the regulation of genes that control inflammation, cell survival, and proliferation. In the context of cancer, aberrant activation and overexpression of RELA are frequently associated with aggressive tumor behavior, therapy resistance, and poorer patient outcomes in cancers such as breast, lung, colorectal, and pancreatic cancers, among others.

RELA emerges as a potential key contributor to the suppression of glycolysis, mitochondrial respiration, and ATP production in cancer cells. (RELA knockdown signifcantly reduced the tumorigenic.
potential of various pancreatic cancer cell lines).
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↓,

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 ⓘ

BAX↑, 1,   Bcl-2↓, 1,   TumCD↓, 1,  

DNA Damage & Repair ⓘ

P53↑, 1,  

Proliferation, Differentiation & Cell State ⓘ

EMT↓, 1,   TumCG↓, 1,  

Migration ⓘ

E-cadherin↑, 1,   Fibronectin↓, 1,   TumCMig↓, 1,   Vim↓, 1,  

Immune & Inflammatory Signaling ⓘ

p65↓, 1,  

Drug Metabolism & Resistance ⓘ

selectivity↑, 1,  
Total Targets: 12

Pathway results for Effect on Normal Cells:


Total Targets: 0

Scientific Paper Hit Count for: p65, RelA
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#:238  State#:%  Dir#:%
  wNotes=0  sortOrder:rid,rpid

 

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