Plumbagin / TumCMig 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)

TumCMig, Tumor cell migration: Click to Expand ⟱

Source:

Type:

Tumor cell migration is a critical process in cancer progression and metastasis, which is the spread of cancer cells from the primary tumor to distant sites in the body.

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↓,

5164-

PLB,

Plumbagin inhibits tumour angiogenesis and tumour growth through the Ras signalling pathway following activation of the VEGF receptor-2

vitro+vivo,

CRC,

Human colon carcinoma and prostate cancer xenograft mouse models were used

in-vitro,

Pca,

TumCP↓, TumCMig↓, angioG↓, VEGFR2↓,

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↑, 1,

Migration ⓘ

MMP9↓, 1, TumCMig↓, 2, TumCP↓, 1,

Angiogenesis & Vasculature ⓘ

angioG↓, 1, VEGFR2↓, 1,
Total Targets: 6

Pathway results for Effect on Normal Cells:

Total Targets: 0

Scientific Paper Hit Count for: TumCMig, Tumor cell migration

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