Emodin / PARP 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)


PARP, poly ADP-ribose polymerase (PARP) cleavage: Click to Expand ⟱
Source:
Type:
Poly (ADP-ribose) polymerase (PARP) cleavage is a hallmark of caspase activation. PARP (Poly (ADP-ribose) polymerase) is a family of proteins involved in a variety of cellular processes, including DNA repair, genomic stability, and programmed cell death. PARP enzymes play a crucial role in repairing single-strand breaks in DNA.
PARP has gained significant attention, particularly in the treatment of certain types of tumors, such as those with BRCA1 or BRCA2 mutations. These mutations impair the cell's ability to repair double-strand breaks in DNA through homologous recombination. Cancer cells with these mutations can become reliant on PARP for survival, making them particularly sensitive to PARP inhibitors.
PARP inhibitors, such as olaparib, rucaparib, and niraparib, have been developed as targeted therapies for cancers associated with BRCA mutations.

PARP Family:
The poly (ADP-ribose) polymerases (PARPs) are a family of enzymes involved in a number of cellular processes, including DNA repair, genomic stability, and programmed cell death.
PARP1 is the predominant family member responsible for detecting DNA strand breaks and initiating repair processes, especially through base excision repair (BER).

PARP1 Overexpression:
In several cancer types—including breast, ovarian, prostate, and lung cancers—elevated PARP1 expression and/or activity has been reported.
High PARP1 expression in certain cancers has been associated with aggressive tumor behavior and resistance to therapies (especially those that induce DNA damage).
Increased PARP1 activity may correlate with poorer overall survival in tumors that rely on DNA repair for survival.
Scientific Papers found: Click to Expand⟱
5225- EMD,    Emodin inhibits growth and induces apoptosis in an orthotopic hepatocellular carcinoma model by blocking activation of STAT3
- vitro+vivo, HCC, HepG2 - in-vitro, HCC, Hep3B - in-vitro, HCC, HUH7
STAT3↓, Akt↓, cSrc↓, JAK1↓, JAK2↓, SHP1↑, cycD1/CCND1↓, Bcl-2↓, Bcl-xL↓, Mcl-1↓, survivin↓, VEGF↓, TumCP↓, Casp3↑, cl‑PARP↑, ChemoSen↑, XIAP↓,
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↓,
1331- EMD,    Aloe-emodin induces apoptosis of human nasopharyngeal carcinoma cells via caspase-8-mediated activation of the mitochondrial death pathway
- in-vitro, NPC, NA
TumCCA↑, CycB/CCNB1↑, DNAdam↑, Casp3↑, cl‑PARP↑, MMP↓, Ca+2↑, ROS↑,
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 ⓘ

MMP↓, 2,   XIAP↓, 1,  

Cell Death ⓘ

Akt↓, 2,   Apoptosis↑, 1,   Bcl-2↓, 2,   Bcl-xL↓, 1,   Casp↑, 1,   Casp3↑, 2,   JNK↓, 1,   MAPK↓, 1,   Mcl-1↓, 1,   survivin↓, 1,   TumCD↑, 1,  

Kinase & Signal Transduction ⓘ

cSrc↓, 1,  

Transcription & Epigenetics ⓘ

tumCV↓, 1,  

DNA Damage & Repair ⓘ

DNAdam↑, 1,   P53↑, 1,   PARP↓, 1,   cl‑PARP↑, 2,  

Cell Cycle & Senescence ⓘ

CycB/CCNB1↑, 1,   cycD1/CCND1↓, 1,   TumCCA↑, 1,  

Proliferation, Differentiation & Cell State ⓘ

Diff↓, 1,   PI3K↓, 1,   SHP1↑, 1,   STAT↓, 1,   STAT3↓, 1,  

Migration ⓘ

Ca+2↑, 1,   TumCP↓, 1,  

Angiogenesis & Vasculature ⓘ

VEGF↓, 1,  

Immune & Inflammatory Signaling ⓘ

JAK1↓, 1,   JAK2↓, 1,   NF-kB↓, 1,  

Drug Metabolism & Resistance ⓘ

ChemoSen↑, 1,   selectivity↑, 1,  
Total Targets: 36

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: PARP, poly ADP-ribose polymerase (PARP) cleavage
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#:239  State#:%  Dir#:%
  wNotes=0  sortOrder:rid,rpid

 

Home Page