VitK3,menadione / JAK1 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)
JAK1, Janus kinase 1: Click to Expand ⟱
Source: CGL-Driver Genes
Type: Oncogene
One of the four members of the Janus kinase family and plays a significant role in the signaling pathways of various cytokines and growth factors, particularly those involved in immune responses. Its involvement in cancer has been increasingly recognized, as dysregulation of JAK1 signaling can contribute to tumorigenesis and cancer progression.
JAK1 is primarily associated with the signaling of several key cytokines, including interleukins (e.g., IL-2, IL-6, IL-10) and interferons. These cytokines are crucial for immune responses, and their dysregulation can lead to inhibitors, such as those targeting JAK1 specifically, are being investigated in clinical trials for various malignancies, including solid tumors and hematological cancers. an environment that supports cancer growth.
Scientific Papers found: Click to Expand⟱
5160- PLB,  VitK3,    Plumbagin, Vitamin K3 Analogue, Suppresses STAT3 Activation Pathway through Induction of Protein Tyrosine Phosphatase, SHP-1: Potential Role in Chemosensitization
- in-vitro, Melanoma, U266
STAT3↓, cSrc↓, JAK1↓, JAK2↓, SHP1↑, cycD1/CCND1↓, Bcl-xL↓, VEGF↓, Casp3↑, cl‑PARP↑, TumCCA↑, ChemoSen↑,

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 ⓘ

Bcl-xL↓, 1,   Casp3↑, 1,  

Kinase & Signal Transduction ⓘ

cSrc↓, 1,  

DNA Damage & Repair ⓘ

cl‑PARP↑, 1,  

Cell Cycle & Senescence ⓘ

cycD1/CCND1↓, 1,   TumCCA↑, 1,  

Proliferation, Differentiation & Cell State ⓘ

SHP1↑, 1,   STAT3↓, 1,  

Angiogenesis & Vasculature ⓘ

VEGF↓, 1,  

Immune & Inflammatory Signaling ⓘ

JAK1↓, 1,   JAK2↓, 1,  

Drug Metabolism & Resistance ⓘ

ChemoSen↑, 1,  
Total Targets: 12

Pathway results for Effect on Normal Cells:


Total Targets: 0

Scientific Paper Hit Count for: JAK1, Janus kinase 1
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#:163  State#:%  Dir#:%
  wNotes=0  sortOrder:rid,rpid

 

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