Plumbagin / CDC2 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)


CDC2, cell division cycle 2: Click to Expand ⟱
Source:
Type:
CDC2 is a gene that encodes a protein known as cyclin-dependent kinase 1 (CDK1), a critical regulator of the cell cycle. CDK1 (historically referred to as CDC2 in some contexts) plays a central role in controlling the transition from the G₂ phase to mitosis (M phase).
Scientific Papers found: Click to Expand⟱
5161- PLB,    Plumbagin induces G2/M arrest, apoptosis, and autophagy via p38 MAPK- and PI3K/Akt/mTOR-mediated pathways in human tongue squamous cell carcinoma cells
- in-vitro, SCC, SCC25
TumCCA↑, Apoptosis↑, TumAuto↑, Bcl-2↓, Bcl-xL↓, BAX↑, PI3K↓, Akt↓, mTOR↓, GSK‐3β↓, MAPK↓, ROS↑, eff↓, CDC2↓, CycB/CCNB1↓, P21↑, p27↑, P53↑, Casp9↑, Casp3↑,
5162- PLB,    Plumbagin induces cell cycle arrest and apoptosis through reactive oxygen species/c-Jun N-terminal kinase pathways in human melanoma A375.S2 cells
- vitro+vivo, Melanoma, A172
TumCG↓, TumCCA↑, Apoptosis↑, P21↑, CycB/CCNB1↓, cycA1/CCNA1↓, CDC2↓, CDC25↑, Bax:Bcl2↑, Casp9↑, ROS↑, JNK↑, ERK↑, eff↓,

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:


Redox & Oxidative Stress ⓘ

ROS↑, 2,  

Mitochondria & Bioenergetics ⓘ

CDC2↓, 2,   CDC25↑, 1,  

Cell Death ⓘ

Akt↓, 1,   Apoptosis↑, 2,   BAX↑, 1,   Bax:Bcl2↑, 1,   Bcl-2↓, 1,   Bcl-xL↓, 1,   Casp3↑, 1,   Casp9↑, 2,   JNK↑, 1,   MAPK↓, 1,   p27↑, 1,  

Autophagy & Lysosomes ⓘ

TumAuto↑, 1,  

DNA Damage & Repair ⓘ

P53↑, 1,  

Cell Cycle & Senescence ⓘ

cycA1/CCNA1↓, 1,   CycB/CCNB1↓, 2,   P21↑, 2,   TumCCA↑, 2,  

Proliferation, Differentiation & Cell State ⓘ

ERK↑, 1,   GSK‐3β↓, 1,   mTOR↓, 1,   PI3K↓, 1,   TumCG↓, 1,  

Drug Metabolism & Resistance ⓘ

eff↓, 2,  
Total Targets: 26

Pathway results for Effect on Normal Cells:


Total Targets: 0

Scientific Paper Hit Count for: CDC2, cell division cycle 2
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#:1323  State#:%  Dir#:1
  wNotes=0  sortOrder:rid,rpid

 

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