Database Query Results : Plumbagin, ,

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)


Scientific Papers found: Click to Expand⟱
1920- JG,  TQ,  PLB,    Natural quinones induce ROS-mediated apoptosis and inhibit cell migration in PANC-1 human pancreatic cancer cell line
- in-vitro, PC, PANC1
ROS↑, TumCMig↓, MMP9↓,
2004- PLB,    Plumbagin Inhibits Proliferative and Inflammatory Responses of T Cells Independent of ROS Generation But by Modulating Intracellular Thiols
- in-vivo, Var, NA
TumCP↓, TumCG↓, NF-kB↓, ROS↑, GSH↓, eff↓, i-Thiols↓, GSH/GSSG↓, *GSH↓, *ROS↑,
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↓,
2006- PLB,    Plumbagin induces apoptosis in human osteosarcoma through ROS generation, endoplasmic reticulum stress and mitochondrial apoptosis pathway
- in-vitro, OS, MG63 - in-vitro, Nor, hFOB1.19
tumCV↓, selectivity↑, mtDam↑, Ca+2↓, ER Stress↑, ROS↑, Casp3↑, Casp9↑, Apoptosis↑, eff↓,
2651- PLB,    Oxidative Stress Inducers in Cancer Therapy: Preclinical and Clinical Evidence
- Review, Var, NA
ROS↑, TrxR↓, GSR↓, ER Stress↓, TumCCA↑, MMP↓, NF-kB↓, PI3K↓, Akt↓, mTOR↓, MKP1↓, MKP2↓, ChemoSen↑,
5158- PLB,    Plumbagin induces reactive oxygen species, which mediate apoptosis in human cervical cancer cells
- in-vitro, Cerv, ME-180
TumCG↓, ROS↑, Apoptosis↑, MMP↓, DNAdam↑, Cyt‑c↑, AIF↑, Casp3↑, Casp9↑, eff↓,
5159- PLB,    Plumbagin treatment leads to apoptosis in human K562 leukemia cells through increased ROS and elevated TRAIL receptor expression
- in-vitro, AML, K562
tumCV↓, Apoptosis↑, ROS↑, eff↓, DR4↑, DR5↑, TRAIL↑,
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↑,
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↓,
5163- PLB,    Plumbagin suppresses epithelial to mesenchymal transition and stemness via inhibiting Nrf2-mediated signaling pathway in human tongue squamous cell carcinoma cells
- in-vitro, SCC, SCC25
TumCP↓, NRF2↓, TumCCA↑, EMT↓, CSCs↓, eff↓, ROS↑, CycB/CCNB1↓, CDK1↓, CDK2↓, CDC25↓, Vim↓, OCT4↓, SOX2↓, Nanog↓, BMI1↓, NQO1↓, GSTA1↓, HSP90↓, toxicity↓,
5164- PLB,    Plumbagin inhibits tumour angiogenesis and tumour growth through the Ras signalling pathway following activation of the VEGF receptor-2
- vitro+vivo, CRC, NA - in-vitro, Pca, NA
TumCP↓, TumCMig↓, angioG↓, VEGFR2↓,

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 12

Pathway results for Effect on Cancer / Diseased Cells:


Redox & Oxidative Stress ⓘ

GSH↓, 1,   GSH/GSSG↓, 2,   GSR↓, 1,   GSTA1↓, 1,   NQO1↓, 1,   NRF2↓, 1,   ROS↑, 11,   mt-ROS↑, 1,   i-Thiols↓, 1,   TrxR↓, 1,  

Mitochondria & Bioenergetics ⓘ

AIF↑, 1,   CDC2↓, 2,   CDC25↓, 1,   CDC25↑, 1,   MMP↓, 2,   mtDam↑, 1,  

Cell Death ⓘ

Akt↓, 2,   Apoptosis↑, 5,   BAX↑, 2,   Bax:Bcl2↑, 1,   Bcl-2↓, 1,   Bcl-xL↓, 2,   Casp3↑, 5,   Casp9↑, 4,   Cyt‑c↑, 3,   DR4↑, 1,   DR5↑, 1,   FasL↑, 1,   JNK↑, 2,   MAPK↓, 1,   MKP1↓, 2,   MKP2↓, 2,   p27↑, 1,   TRAIL↑, 1,  

Kinase & Signal Transduction ⓘ

cSrc↓, 1,  

Transcription & Epigenetics ⓘ

tumCV↓, 2,   tumCV↑, 1,  

Protein Folding & ER Stress ⓘ

ER Stress↓, 1,   ER Stress↑, 1,   HSP90↓, 1,  

Autophagy & Lysosomes ⓘ

TumAuto↑, 1,  

DNA Damage & Repair ⓘ

DNAdam↑, 1,   P53↑, 1,   cl‑PARP↑, 1,  

Cell Cycle & Senescence ⓘ

CDK1↓, 1,   CDK2↓, 1,   cycA1/CCNA1↓, 1,   CycB/CCNB1↓, 3,   cycD1/CCND1↓, 1,   P21↑, 2,   TumCCA↑, 5,  

Proliferation, Differentiation & Cell State ⓘ

BMI1↓, 1,   CSCs↓, 1,   EMT↓, 1,   ERK↑, 1,   GSK‐3β↓, 1,   mTOR↓, 2,   Nanog↓, 1,   OCT4↓, 1,   PI3K↓, 2,   SHP1↑, 1,   SOX2↓, 1,   STAT3↓, 1,   TumCG↓, 3,  

Migration ⓘ

Ca+2↓, 1,   MMP9↓, 1,   TumCMig↓, 2,   TumCP↓, 3,   Vim↓, 1,  

Angiogenesis & Vasculature ⓘ

angioG↓, 1,   VEGF↓, 1,   VEGFR2↓, 1,  

Immune & Inflammatory Signaling ⓘ

JAK1↓, 1,   JAK2↓, 1,   NF-kB↓, 2,  

Drug Metabolism & Resistance ⓘ

ChemoSen↑, 2,   eff↓, 8,   selectivity↑, 1,   selectivity∅, 1,  

Functional Outcomes ⓘ

toxicity↓, 1,  
Total Targets: 80

Pathway results for Effect on Normal Cells:


Redox & Oxidative Stress ⓘ

GSH↓, 1,   ROS↑, 3,  
Total Targets: 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#:%  State#:%  Dir#:%
  wNotes=0  sortOrder:rid,rpid

 

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