Plumbagin / tumCV Cancer Research Results

PLB, Plumbagin: Click to Expand ⟱
Features:
Plumbagin (5-hydroxy-2-methyl-1,4-naphthoquinone) is a naturally occurring naphthoquinone derivative.

–Plumbagin can undergo redox cycling to generate reactive oxygen species (ROS)
-apototosis, activation of caspases, modulation of Bax, Bcl‑2, loss of MMP.
-Cell cycle arrest in cancer cells, often at the G0/G1, or G2/M phases.
-May inhibit NF‑κB activation
– MAPK Pathways
– PI3K/Akt Pathway
-Downregulation of (VEGF) and matrix metalloproteinases (MMPs).

-Seems capable of raising ROS in normal and cancer cells (#2004)

-ic50 cancer cells 1-10uM, normal cells >10uM

Rank Pathway / Target Axis Direction Primary Effect Notes / Cancer Relevance Ref
1 Oxidative stress (redox cycling) ↑ ROS Upstream cytotoxic trigger Plumbagin induces ROS; ROS generation is causally linked to cell death in cancer models (ref)
2 Mitochondrial integrity (ΔΨm) ↓ ΔΨm Mitochondrial dysfunction Loss of mitochondrial membrane potential occurs during plumbagin-induced apoptotic progression (ref)
3 Intrinsic apoptosis (caspase cascade) ↑ caspase-dependent apoptosis Programmed cell death Plumbagin triggers apoptosis in leukemia and solid tumor cells; antioxidant rescue attenuates killing (ref)
4 NF-κB signaling ↓ NF-κB activation Reduced pro-survival / inflammatory transcription Demonstrates plumbagin suppresses NF-κB signaling in tumor/immune contexts (direction explicitly shown) (ref)
5 STAT3 signaling ↓ STAT3 phosphorylation Reduced survival & proliferation signaling Plumbagin suppresses constitutive and inducible STAT3 phosphorylation in cancer cells (ref)
6 PI3K–AKT–mTOR signaling ↓ PI3K/AKT/mTOR activity Survival pathway suppression Plumbagin inhibits PI3K/AKT/mTOR signaling in cancer cells with linked apoptosis/autophagy outcomes (ref)
7 Autophagy program ↑ autophagy Stress response (context-dependent role) Plumbagin induces autophagy alongside apoptosis; pathway involvement (p38, PI3K/AKT/mTOR) is demonstrated (ref)
8 Stress MAPK (p38 MAPK) ↑ p38 activation Stress signaling amplification p38 MAPK activation is implicated in plumbagin-driven apoptosis/autophagy signaling in cancer cells (ref)
9 Cell cycle control ↑ G2/M (or S–G2/M) arrest Proliferation blockade Plumbagin induces checkpoint arrest with changes in cyclins/CDKs consistent with growth inhibition (ref)
10 Death receptor axis (TRAIL receptors DR4/DR5) ↑ DR4/DR5 expression Sensitizes to TRAIL-mediated killing Plumbagin increases DR4/DR5 and enhances TRAIL killing; NAC blocks both ROS and receptor upregulation (ref)
11 EMT / invasion programs ↓ EMT (anti-invasive) Reduced metastasis-related phenotype Plumbagin suppresses epithelial–mesenchymal transition and stemness-related markers in cancer cells (ref)
12 Angiogenesis signaling (VEGFR2/VEGF-driven endothelial responses) ↓ angiogenesis signaling / function Anti-angiogenic effect Plumbagin inhibits tumor angiogenesis via interference with VEGFR2-mediated signaling in endothelial/tumor models (ref)


tumCV, Cell Viability: Click to Expand ⟱
Source:
Type:
Cell Viability
Scientific Papers found: Click to Expand⟱
2005- PLB,    Plumbagin induces apoptosis in lymphoma cells via oxidative stress mediated glutathionylation and inhibition of mitogen-activated protein kinase phosphatases (MKP1/2)
- in-vivo, Nor, EL4 - in-vitro, AML, Jurkat
JNK↑, Cyt‑c↑, FasL↑, BAX↑, ROS↑, *ROS↑, MKP1↓, MKP2↓, selectivity∅, tumCV↑, Cyt‑c↑, Casp3↑, GSH/GSSG↓, ROS↑, mt-ROS↑, *ROS↑, eff↓,

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 ⓘ

GSH/GSSG↓, 1,   ROS↑, 2,   mt-ROS↑, 1,  

Cell Death ⓘ

BAX↑, 1,   Casp3↑, 1,   Cyt‑c↑, 2,   FasL↑, 1,   JNK↑, 1,   MKP1↓, 1,   MKP2↓, 1,  

Transcription & Epigenetics ⓘ

tumCV↑, 1,  

Drug Metabolism & Resistance ⓘ

eff↓, 1,   selectivity∅, 1,  
Total Targets: 13

Pathway results for Effect on Normal Cells:


Redox & Oxidative Stress ⓘ

ROS↑, 2,  
Total Targets: 1

Scientific Paper Hit Count for: tumCV, Cell Viability
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#:299  Target#:897  State#:%  Dir#:2
  wNotes=0  sortOrder:rid,rpid

 

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