Emodin / MMP 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)

MMP, ΔΨm, mitochondrial membrane potential: Click to Expand ⟱

Source:

Type:

Destruction of mitochondrial transmembrane potential, which is widely regarded as one of the earliest events in the process of cell apoptosis.
Mitochondria are organelles within eukaryotic cells that produce adenosine triphosphate (ATP), the main energy molecule used by the cell. For this reason, the mitochondrion is sometimes referred to as “the powerhouse of the cell”.
Mitochondria produce ATP through process of cellular respiration—specifically, aerobic respiration, which requires oxygen. The citric acid cycle, or Krebs cycle, takes place in the mitochondria.
The mitochondrial membrane potential is widely used in assessing mitochondrial function as it relates to the mitochondrial capacity of ATP generation by oxidative phosphorylation. The mitochondrial membrane potential is a reliable indicator of mitochondrial health.
In cancer cells, ΔΨm is often decreased, which can lead to changes in cellular metabolism, increased glycolysis, increased reactive oxygen species (ROS) production, and altered cell death pathways.

The membrane of malignant mitochondria is hyperpolarized (−220 mV) in comparison to their healthy counterparts (−160 mV), which facilitates the penetration of positively charged molecules to the cancer cells mitochondria.
The MMP is a critical indicator of mitochondrial function, directly reflecting the organelle's capacity to generate ATP through oxidative phosphorylation.

Scientific Papers found: Click to Expand⟱

1327-

EMD,

Emodin induces apoptosis in human lung adenocarcinoma cells through a reactive oxygen species-dependent mitochondrial signaling pathway

in-vitro,

Lung,

A549

50uM

Cyt‑c↑, Casp2↑, Casp3↑, Casp9↑, ERK↓, Akt↓, ROS↑, MMP↓, Bcl-2↓, BAX↑,

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

rata

*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,

TumCCA↑, CycB/CCNB1↑, DNAdam↑, Casp3↑, cl‑PARP↑, MMP↓, Ca+2↑, ROS↑,

1330-

EMD,

Aloe emodin-induced apoptosis in t-HSC/Cl-6 cells involves a mitochondria-mediated pathway

in-vitro,

NA,

12.5, 25, or 50 microM

tumCV↓, Casp3↑, Casp9↑, MMP↓, Cyt‑c↑, BAX↑, Bax:Bcl2↑,

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

30 microM

TumCCA↑, eff↓, P53↑, P21↑, p27↑, cycA1/CCNA1↓, cycE/CCNE↓, TS↓, CDC25↓, AIF↑, proCasp9↓, Cyt‑c↑, MMP↓, Bax:Bcl2↑, Casp3↑, Casp9↑,

1328-

EMD,

Emodin induces apoptosis of human tongue squamous cancer SCC-4 cells through reactive oxygen species and mitochondria-dependent pathways

in-vitro,

Tong,

SCC4

TumCCA↑, P21↑, Chk2↑, CycB/CCNB1↓, cDC2↓, Apoptosis↑, Cyt‑c↑, Casp9↑, Casp3↑, ROS↑, MMP↓, Bax:Bcl2↑, ER Stress↑,

1324-

EMD,

Is Emodin with Anticancer Effects Completely Innocent? Two Sides of the Coin

Review,

Var,

2–10 μM

*toxicity↑, *BioAv↓, Akt↓, ERK↓, ROS↑, MMP↓, Bcl-2↓, BAX↑, TumCCA↑,

1323-

EMD,

Anticancer action of naturally occurring emodin for the controlling of cervical cancer

Review,

Cerv,

56.7 µmol/L

TumCCA↑, DNAdam↑, mTOR↓, Casp3↑, Casp8↑, Casp9↑, TGF-β↑, SMAD3↓, p‑SMAD4↓, ROS↑, MMP↓, CXCR4↓, HER2/EBBR2↓, ER Stress↓, TumAuto↑, NOTCH1↓,

1321-

EMD,

Antitumor effects of emodin on LS1034 human colon cancer cells in vitro and in vivo: roles of apoptotic cell death and LS1034 tumor xenografts model

in-vitro,

CRC,

LS1034

in-vivo,

NA,

mice

tumCV↓, TumCCA↑, ROS↑, Ca+2↑, MMP↓, Apoptosis↑, Cyt‑c↑, Casp9↑, Bax:Bcl2↑,

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↑,

1296-

EMD,

Emodin inhibits LOVO colorectal cancer cell proliferation via the regulation of the Bcl-2/Bax ratio and cytochrome c

in-vitro,

CRC,

LoVo

BAX↑, Bcl-2↓, MMP↓, Cyt‑c↑,

1245-

EMD,

Emodin Exhibits Strong Cytotoxic Effect in Cervical Cancer Cells by Activating Intrinsic Pathway of Apoptosis

in-vitro,

Cerv,

HeLa

10-50 μM

20uM@48hr

TumCG↓, TumCP↓, Apoptosis↑, ROS↑, Casp3↑, Casp9↑, MMP↓, DNAdam↑, GSH↓,

Showing Research Papers: 1 to 13 of 13

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 13

Pathway results for Effect on Cancer / Diseased Cells:

Clinical Biomarkers ⓘ

HER2/EBBR2↓, 1,
Total Targets: 56

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,

Drug Metabolism & Resistance ⓘ

BioAv↓, 1,

Functional Outcomes ⓘ

toxicity↑, 1,
Total Targets: 21

Scientific Paper Hit Count for: MMP, ΔΨm, mitochondrial membrane potential

13 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#:197  State#:%  Dir#:1
  wNotes=0  sortOrder:rid,rpid

Emodin / MMP Cancer Research Results

Pathway results for Effect on Cancer / Diseased Cells:

Redox & Oxidative Stress ⓘ

Mitochondria & Bioenergetics ⓘ

Core Metabolism/Glycolysis ⓘ

Cell Death ⓘ

Kinase & Signal Transduction ⓘ

Transcription & Epigenetics ⓘ

Protein Folding & ER Stress ⓘ

Autophagy & Lysosomes ⓘ

DNA Damage & Repair ⓘ

Cell Cycle & Senescence ⓘ

Proliferation, Differentiation & Cell State ⓘ

Migration ⓘ

Immune & Inflammatory Signaling ⓘ

Drug Metabolism & Resistance ⓘ

Clinical Biomarkers ⓘ

Pathway results for Effect on Normal Cells:

Redox & Oxidative Stress ⓘ

Mitochondria & Bioenergetics ⓘ

Cell Death ⓘ

Transcription & Epigenetics ⓘ

DNA Damage & Repair ⓘ

Cell Cycle & Senescence ⓘ

Drug Metabolism & Resistance ⓘ

Functional Outcomes ⓘ

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