Emodin / P53 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)


P53, P53-Guardian of the Genome: Click to Expand ⟱
Source: TCGA
Type: Proapototic
TP53 is the most commonly mutated gene in human cancer. TP53 is a gene that encodes for the p53 tumor suppressor protein ; TP73 (Chr.1p36.33) and TP63 (Chr.3q28) genes that encode transcription factors p73 and p63, respectively, are TP53 homologous structures.
p53 is a crucial tumor suppressor protein that plays a significant role in regulating the cell cycle, maintaining genomic stability, and preventing tumor formation. It is often referred to as the "guardian of the genome" due to its role in protecting cells from DNA damage and stress.
TP53 gene, which encodes the p53 protein, is one of the most frequently mutated genes in human cancers.
Overexpression of MDM2, an inhibitor of p53, can lead to decreased p53 activity even in the presence of wild-type p53.
In some cancers, particularly those with mutant p53, there may be an overexpression of the p53 protein.
Cancers with overexpression: Breast, lung, colorectal, overian, head and neck, Esophageal, bladder, pancreatic, and liver.
Scientific Papers found: Click to Expand⟱
5223- EMD,    Emodin inhibits colon cancer by altering BCL-2 family proteins and cell survival pathways
- in-vitro, CRC, DLD1 - in-vitro, Nor, CCD841
tumCV↓, Apoptosis↑, selectivity↑, Casp↑, Bcl-2↓, MMP↓, TumCD↑, MAPK↓, JNK↓, PI3K↓, Akt↓, NF-kB↓, STAT↓, Diff↓, P53↑, PARP↓,
1332- EMD,    Induction of Apoptosis in HepaRG Cell Line by Aloe-Emodin through Generation of Reactive Oxygen Species and the Mitochondrial Pathway
- in-vivo, Nor, HepaRG
*tumCV↓, *ROS↑, *MMP↓, *Fas↑, *P53↑, *P21↑, *Bax:Bcl2↑, *Casp3↑, *Casp8↑, *Casp9↑, *cl‑PARP↑, *TumCCA↑, *P21↑, *cycE/CCNE↑, *cycA1/CCNA1↓, *CDK2↓,
1329- EMD,    Aloe-emodin induces cell death through S-phase arrest and caspase-dependent pathways in human tongue squamous cancer SCC-4 cells
- in-vitro, Tong, SCC4
TumCCA↑, eff↓, P53↑, P21↑, p27↑, cycA1/CCNA1↓, cycE/CCNE↓, TS↓, CDC25↓, AIF↑, proCasp9↓, Cyt‑c↑, MMP↓, Bax:Bcl2↑, Casp3↑, Casp9↑,
1326- EMD,    Emodin induces a reactive oxygen species-dependent and ATM-p53-Bax mediated cytotoxicity in lung cancer cells
- in-vitro, Lung, A549
Apoptosis↑, ROS↑, P53↑, BAX↑, ATM↑,
1318- EMD,    Aloe-emodin Induces Apoptosis in Human Liver HL-7702 Cells through Fas Death Pathway and the Mitochondrial Pathway by Generating Reactive Oxygen Species
- in-vitro, Nor, HL7702
*TumCCA↑, *ROS↑, *MMP↓, *Fas↑, *P53↑, *P21↓, *Bax:Bcl2↑, *cl‑Casp3↑, *cl‑Casp8↑, *cl‑Casp9↑, *cl‑PARP↑,

Showing Research Papers: 1 to 5 of 5

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 5

Pathway results for Effect on Cancer / Diseased Cells:


Redox & Oxidative Stress ⓘ

ROS↑, 1,  

Mitochondria & Bioenergetics ⓘ

AIF↑, 1,   CDC25↓, 1,   MMP↓, 2,  

Core Metabolism/Glycolysis ⓘ

TS↓, 1,  

Cell Death ⓘ

Akt↓, 1,   Apoptosis↑, 2,   BAX↑, 1,   Bax:Bcl2↑, 1,   Bcl-2↓, 1,   Casp↑, 1,   Casp3↑, 1,   Casp9↑, 1,   proCasp9↓, 1,   Cyt‑c↑, 1,   JNK↓, 1,   MAPK↓, 1,   p27↑, 1,   TumCD↑, 1,  

Transcription & Epigenetics ⓘ

tumCV↓, 1,  

DNA Damage & Repair ⓘ

ATM↑, 1,   P53↑, 3,   PARP↓, 1,  

Cell Cycle & Senescence ⓘ

cycA1/CCNA1↓, 1,   cycE/CCNE↓, 1,   P21↑, 1,   TumCCA↑, 1,  

Proliferation, Differentiation & Cell State ⓘ

Diff↓, 1,   PI3K↓, 1,   STAT↓, 1,  

Immune & Inflammatory Signaling ⓘ

NF-kB↓, 1,  

Drug Metabolism & Resistance ⓘ

eff↓, 1,   selectivity↑, 1,  
Total Targets: 33

Pathway results for Effect on Normal Cells:


Redox & Oxidative Stress ⓘ

ROS↑, 2,  

Mitochondria & Bioenergetics ⓘ

MMP↓, 2,  

Cell Death ⓘ

Bax:Bcl2↑, 2,   Casp3↑, 1,   cl‑Casp3↑, 1,   Casp8↑, 1,   cl‑Casp8↑, 1,   Casp9↑, 1,   cl‑Casp9↑, 1,   Fas↑, 2,  

Transcription & Epigenetics ⓘ

tumCV↓, 1,  

DNA Damage & Repair ⓘ

P53↑, 2,   cl‑PARP↑, 2,  

Cell Cycle & Senescence ⓘ

CDK2↓, 1,   cycA1/CCNA1↓, 1,   cycE/CCNE↑, 1,   P21↓, 1,   P21↑, 2,   TumCCA↑, 2,  
Total Targets: 19

Scientific Paper Hit Count for: P53, P53-Guardian of the Genome
5 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#:236  State#:%  Dir#:2
  wNotes=0  sortOrder:rid,rpid

 

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