Emodin / TGF-β Cancer Research Results

EMD, Emodin: Click to Expand ⟱
Features:
Organic compound isolated from rhubarb, buckthorn, knotweed. It has laxative, anticancer, antibacterial, antiinflammatory, and antiviral activities, and is used in traditional Chinese medicine.
Emodin, an anthraquinone derivative found in various plants (e.g., rhubarb, Polygonum cuspidatum).

Pathways:
- Generation of Reactive Oxygen Species (ROS)
- Upregulation Bax downregulation of Bcl‑2, caspase activation and cyt_c release.
- Induce cell cycle arrest at various checkpoints (commonly G0/G1 or G2/M phases.
- Can inhibit NF‑κB activation
– MAPK Pathways
– PI3K/Akt Pathway
- Metalloproteinases (MMPs)

-ic50 cancer cells 10-50uM, normal cells higher(supports a therapeutic window)

Rank Pathway / Target Axis Direction Label Primary Effect Notes / Cancer Relevance Ref
1 Reactive oxygen species (ROS) ↑ ROS Driver Upstream cytotoxic trigger Emodin induces ROS in cancer cells; ROS increase is positioned upstream of mitochondrial dysfunction and death signaling. (ref)
2 Mitochondrial integrity (ΔΨm) ↓ ΔΨm Driver Mitochondrial dysfunction Emodin decreases mitochondrial membrane potential (ΔΨm), consistent with mitochondria-dependent killing. (ref)
3 Intrinsic apoptosis (caspase cascade) ↑ apoptosis (↑ caspases / ↑ PARP cleavage) Driver Execution-phase cell death Emodin activates caspase-dependent apoptosis with mitochondrial involvement in colon cancer models. (ref)
4 AMPK → AKT/mTOR axis ↑ AMPK / ↓ AKT-mTOR signaling Secondary Growth/metabolic suppression NSCLC study reports AMPK activation with inhibition of AKT/mTOR alongside apoptosis and ROS increase (consistent directionality). (ref)
5 NF-κB signaling ↓ NF-κB activation (↓ p65 nuclear translocation; ↓ IκBα phosphorylation/degradation) Secondary Reduced pro-survival/inflammatory transcription Emodin inhibits TNF-α–induced NF-κB activation by blocking IκBα phosphorylation/degradation and p65 nuclear activity. (ref)
6 STAT3 signaling ↓ STAT3 activation (↓ phosphorylation) Secondary Reduced survival/proliferation signaling HCC study shows emodin suppresses STAT3 activation (and discusses upstream kinase modulation), supporting directionality as STAT3↓. (ref)
7 HIF-1α hypoxia program ↓ HIF-1α (↓ biosynthesis; not via transcription/stability) Adaptive Reduced hypoxia tolerance Pancreatic cancer study: emodin decreases HIF-1α by decreasing biosynthesis (explicit mechanism stated). (ref)
8 Aerobic glycolysis (Warburg output) ↓ glycolysis (↓ ECAR / ↓ glycolytic dependence) Phenotypic Metabolic suppression Renal cancer paper reports emodin inhibits aerobic glycolysis (and links killing to a non-apoptotic death mode in that model). (ref)
9 HDAC inhibition (epigenetic enzyme activity) ↓ HDAC activity Secondary Epigenetic modulation Direct biochemical evidence: emodin inhibits HDAC activity in vitro (fast-on/slow-off kinetics reported). (ref)
10 NRF2 / HO-1 antioxidant response ↑ NRF2 / ↑ HO-1 (context-dependent stress response) Adaptive Counter-response to redox stress HCC model reports emodin increases NRF2 and HO-1 expression; interpret as adaptive/compensatory (not necessarily the cytotoxic driver). (ref)


TGF-β, transforming growth factor-beta: Click to Expand ⟱
Source: HalifaxProj(inhibit) CGL-CS TCGA
Type:
Human malignancies frequently exhibit mutations in the TGF-β pathway, and overactivation of this system is linked to tumor growth by promoting angiogenesis and inhibiting the innate and adaptive antitumor immune responses.
Anti-inflammatory cytokine.
In normal tissues, TGF-β plays an essential role in cell cycle regulation, immune function, and tissue remodeling.
- In early carcinogenesis, TGF-β typically acts as a tumor suppressor by inhibiting cell proliferation and inducing apoptosis.

In advanced cancers, cells frequently become resistant to the growth-inhibitory effects of TGF-β.
- TGF-β then switches roles and promotes tumor progression by stimulating epithelial-to-mesenchymal transition (EMT), cell invasion, metastasis, and immune evasion.

Non-canonical (Smad-independent) pathways, such as MAPK, PI3K/Akt, and Rho signaling, also contribute to TGF-β-mediated responses.

Elevated levels of TGF-β have been detected in many advanced-stage cancers, including breast, lung, colorectal, pancreatic, and prostate cancers.
 - The switch from a tumor-suppressive to a tumor-promoting role is often associated with increased TGF-β production and activation in the tumor microenvironment.

High TGF-β expression or signaling activity is frequently correlated with aggressive disease features, resistance to therapy, increased metastasis, and poorer overall survival in many cancer types.
Scientific Papers found: Click to Expand⟱
1323- EMD,    Anticancer action of naturally occurring emodin for the controlling of cervical cancer
- Review, Cerv, NA
TumCCA↑, DNAdam↑, mTOR↓, Casp3↑, Casp8↑, Casp9↑, TGF-β↑, SMAD3↓, p‑SMAD4↓, ROS↑, MMP↓, CXCR4↓, HER2/EBBR2↓, ER Stress↓, TumAuto↑, NOTCH1↓,
1322- EMD,    The versatile emodin: A natural easily acquired anthraquinone possesses promising anticancer properties against a variety of cancers
- Review, Var, NA
Apoptosis↑, TumCP↓, ROS↑, TumAuto↑, EMT↓, TGF-β↓, DNAdam↑, ER Stress↑, TumCCA↑, ATP↓, NF-kB↓, CYP1A1↑, STAC2↓, JAK↓, PI3K↓, Akt↓, MAPK↓, FASN↓, HER2/EBBR2↓, ChemoSen↑, eff↑, ChemoSen↑, angioG↓, VEGF↓, MMP2↓, eNOS↓, FOXD3↑, MMP9↓, TIMP1↑,
1246- EMD,    Emodin reduces Breast Cancer Lung Metastasis by suppressing Macrophage-induced Breast Cancer Cell Epithelial-mesenchymal transition and Cancer Stem Cell formation
- in-vivo, BC, NA
TGF-β↓, EMT↓, CSCs↓,

Showing Research Papers: 1 to 3 of 3

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 3

Pathway results for Effect on Cancer / Diseased Cells:


Redox & Oxidative Stress ⓘ

CYP1A1↑, 1,   ROS↑, 2,  

Mitochondria & Bioenergetics ⓘ

ATP↓, 1,   MMP↓, 1,  

Core Metabolism/Glycolysis ⓘ

FASN↓, 1,  

Cell Death ⓘ

Akt↓, 1,   Apoptosis↑, 1,   Casp3↑, 1,   Casp8↑, 1,   Casp9↑, 1,   MAPK↓, 1,  

Kinase & Signal Transduction ⓘ

FOXD3↑, 1,   HER2/EBBR2↓, 2,  

Protein Folding & ER Stress ⓘ

ER Stress↓, 1,   ER Stress↑, 1,  

Autophagy & Lysosomes ⓘ

TumAuto↑, 2,  

DNA Damage & Repair ⓘ

DNAdam↑, 2,  

Cell Cycle & Senescence ⓘ

TumCCA↑, 2,  

Proliferation, Differentiation & Cell State ⓘ

CSCs↓, 1,   EMT↓, 2,   mTOR↓, 1,   NOTCH1↓, 1,   PI3K↓, 1,  

Migration ⓘ

MMP2↓, 1,   MMP9↓, 1,   SMAD3↓, 1,   p‑SMAD4↓, 1,   STAC2↓, 1,   TGF-β↓, 2,   TGF-β↑, 1,   TIMP1↑, 1,   TumCP↓, 1,  

Angiogenesis & Vasculature ⓘ

angioG↓, 1,   eNOS↓, 1,   VEGF↓, 1,  

Immune & Inflammatory Signaling ⓘ

CXCR4↓, 1,   JAK↓, 1,   NF-kB↓, 1,  

Drug Metabolism & Resistance ⓘ

ChemoSen↑, 2,   eff↑, 1,  

Clinical Biomarkers ⓘ

HER2/EBBR2↓, 2,  
Total Targets: 41

Pathway results for Effect on Normal Cells:


Total Targets: 0

Scientific Paper Hit Count for: TGF-β, transforming growth factor-beta
3 Emodin
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#:75  Target#:304  State#:%  Dir#:%
  wNotes=0  sortOrder:rid,rpid

 

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