tbResList Print — EMD Emodin

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Product

EMD Emodin
Description: </b>Organic</b> compound isolated from rhubarb, buckthorn, knotweed. It has laxative, anticancer, antibacterial, antiinflammatory, and antiviral activities, and is used in traditional Chinese medicine.<br>
Emodin, an anthraquinone derivative found in various plants (e.g., rhubarb, Polygonum cuspidatum).<br>
<br>
Pathways:<br>
- Generation of Reactive Oxygen Species (ROS)<br>
- Upregulation Bax downregulation of Bcl‑2, caspase activation and cyt_c release.<br>
- Induce cell cycle arrest at various checkpoints (commonly G0/G1 or G2/M phases.<br>
- Can inhibit NF‑κB activation<br>
– MAPK Pathways<br>
– PI3K/Akt Pathway<br>
- Metalloproteinases (MMPs) <br>
<br>
-ic50 cancer cells 10-50uM, normal cells higher(supports a therapeutic window)<br>

<br>

<table border="1" cellspacing="0" cellpadding="4">
<tr>
<th>Rank</th>
<th>Pathway / Target Axis</th>
<th>Direction</th>
<th>Label</th>
<th>Primary Effect</th>
<th>Notes / Cancer Relevance</th>
<th>Ref</th>
</tr>

<tr>
<td>1</td>
<td>Reactive oxygen species (ROS)</td>
<td>↑ ROS</td>
<td>Driver</td>
<td>Upstream cytotoxic trigger</td>
<td>Emodin induces ROS in cancer cells; ROS increase is positioned upstream of mitochondrial dysfunction and death signaling.</td>
<td><a href="https://ar.iiarjournals.org/content/29/1/327">(ref)</a></td>
</tr>

<tr>
<td>2</td>
<td>Mitochondrial integrity (ΔΨm)</td>
<td>↓ ΔΨm</td>
<td>Driver</td>
<td>Mitochondrial dysfunction</td>
<td>Emodin decreases mitochondrial membrane potential (ΔΨm), consistent with mitochondria-dependent killing.</td>
<td><a href="https://ar.iiarjournals.org/content/29/1/327">(ref)</a></td>
</tr>

<tr>
<td>3</td>
<td>Intrinsic apoptosis (caspase cascade)</td>
<td>↑ apoptosis (↑ caspases / ↑ PARP cleavage)</td>
<td>Driver</td>
<td>Execution-phase cell death</td>
<td>Emodin activates caspase-dependent apoptosis with mitochondrial involvement in colon cancer models.</td>
<td><a href="https://link.springer.com/article/10.1186/s12935-019-0820-3">(ref)</a></td>
</tr>

<tr>
<td>4</td>
<td>AMPK → AKT/mTOR axis</td>
<td>↑ AMPK / ↓ AKT-mTOR signaling</td>
<td>Secondary</td>
<td>Growth/metabolic suppression</td>
<td>NSCLC study reports AMPK activation with inhibition of AKT/mTOR alongside apoptosis and ROS increase (consistent directionality).</td>
<td><a href="https://pubmed.ncbi.nlm.nih.gov/34785104/">(ref)</a></td>
</tr>

<tr>
<td>5</td>
<td>NF-κB signaling</td>
<td>↓ NF-κB activation (↓ p65 nuclear translocation; ↓ IκBα phosphorylation/degradation)</td>
<td>Secondary</td>
<td>Reduced pro-survival/inflammatory transcription</td>
<td>Emodin inhibits TNF-α–induced NF-κB activation by blocking IκBα phosphorylation/degradation and p65 nuclear activity.</td>
<td><a href="https://pmc.ncbi.nlm.nih.gov/articles/PMC3879914/">(ref)</a></td>
</tr>

<tr>
<td>6</td>
<td>STAT3 signaling</td>
<td>↓ STAT3 activation (↓ phosphorylation)</td>
<td>Secondary</td>
<td>Reduced survival/proliferation signaling</td>
<td>HCC study shows emodin suppresses STAT3 activation (and discusses upstream kinase modulation), supporting directionality as STAT3↓.</td>
<td><a href="https://pmc.ncbi.nlm.nih.gov/articles/PMC3799595/">(ref)</a></td>
</tr>

<tr>
<td>7</td>
<td>HIF-1α hypoxia program</td>
<td>↓ HIF-1α (↓ biosynthesis; not via transcription/stability)</td>
<td>Adaptive</td>
<td>Reduced hypoxia tolerance</td>
<td>Pancreatic cancer study: emodin decreases HIF-1α by decreasing biosynthesis (explicit mechanism stated).</td>
<td><a href="https://pmc.ncbi.nlm.nih.gov/articles/PMC5675689/">(ref)</a></td>
</tr>

<tr>
<td>8</td>
<td>Aerobic glycolysis (Warburg output)</td>
<td>↓ glycolysis (↓ ECAR / ↓ glycolytic dependence)</td>
<td>Phenotypic</td>
<td>Metabolic suppression</td>
<td>Renal cancer paper reports emodin inhibits aerobic glycolysis (and links killing to a non-apoptotic death mode in that model).</td>
<td><a href="https://pmc.ncbi.nlm.nih.gov/articles/PMC7837784/">(ref)</a></td>
</tr>

<tr>
<td>9</td>
<td>HDAC inhibition (epigenetic enzyme activity)</td>
<td>↓ HDAC activity</td>
<td>Secondary</td>
<td>Epigenetic modulation</td>
<td>Direct biochemical evidence: emodin inhibits HDAC activity in vitro (fast-on/slow-off kinetics reported).</td>
<td><a href="https://pmc.ncbi.nlm.nih.gov/articles/PMC7162729/">(ref)</a></td>
</tr>

<tr>
<td>10</td>
<td>NRF2 / HO-1 antioxidant response</td>
<td>↑ NRF2 / ↑ HO-1 (context-dependent stress response)</td>
<td>Adaptive</td>
<td>Counter-response to redox stress</td>
<td>HCC model reports emodin increases NRF2 and HO-1 expression; interpret as adaptive/compensatory (not necessarily the cytotoxic driver).</td>
<td><a href="https://pmc.ncbi.nlm.nih.gov/articles/PMC11168332/">(ref)</a></td>
</tr>

</table>

Pathway results for Effect on Cancer / Diseased Cells

Redox & Oxidative Stress ⓘ

CYP1A1↑, 1,   GSH↓, 1,   HO-1↑, 1,   MDA↓, 1,   NRF2↑, 1,   ROS↑, 9,   ROS↓, 1,  

Mitochondria & Bioenergetics ⓘ

AIF↑, 1,   ATP↓, 1,   CDC25↓, 1,   MMP↓, 11,   XIAP↓, 1,  

Core Metabolism/Glycolysis ⓘ

FASN↓, 1,   glut↓, 1,   Glycolysis↓, 1,   HK2↓, 1,   LDHA↓, 1,   PKM2↓, 1,   SREBF2↓, 1,   TS↓, 1,  

Cell Death ⓘ

Akt↓, 6,   p‑Akt↓, 1,   Apoptosis↑, 7,   BAX↑, 6,   Bax:Bcl2↑, 4,   Bcl-2↓, 6,   Bcl-xL↓, 1,   Casp↑, 1,   Casp2↑, 1,   Casp3↑, 9,   Casp8↑, 1,   Casp9↑, 7,   proCasp9↓, 1,   Chk2↑, 1,   Cyt‑c↑, 6,   JNK↓, 1,   MAPK↓, 2,   p‑MAPK↓, 1,   Mcl-1↓, 1,   MLKL↑, 1,   Necroptosis↑, 1,   p27↑, 1,   p‑RIP1↑, 1,   survivin↓, 1,   TumCD↑, 1,  

Kinase & Signal Transduction ⓘ

cSrc↓, 1,   FOXD3↑, 1,   HER2/EBBR2↓, 2,  

Transcription & Epigenetics ⓘ

ac‑H3↑, 1,   tumCV↓, 3,  

Protein Folding & ER Stress ⓘ

ER Stress↑, 2,   ER Stress↓, 1,  

Autophagy & Lysosomes ⓘ

TumAuto↑, 2,  

DNA Damage & Repair ⓘ

ATM↑, 1,   DNAdam↑, 4,   P53↑, 3,   cl‑PARP↑, 2,   PARP↓, 1,  

Cell Cycle & Senescence ⓘ

cycA1/CCNA1↓, 1,   CycB/CCNB1↓, 1,   CycB/CCNB1↑, 1,   cycD1/CCND1↓, 1,   cycE/CCNE↓, 1,   P21↑, 2,   TumCCA↑, 9,  

Proliferation, Differentiation & Cell State ⓘ

CD133↓, 1,   cDC2↓, 1,   CSCs↓, 2,   Diff↓, 1,   EMT↓, 3,   ERK↓, 3,   p‑ERK↓, 1,   ERK5↓, 1,   HDAC↓, 1,   HDAC1↓, 1,   HDAC2↓, 1,   mTOR↓, 1,   NOTCH1↓, 1,   OCT4↓, 1,   PI3K↓, 2,   SHP1↑, 1,   STAT↓, 1,   STAT3↓, 2,   TumCG↓, 4,  

Migration ⓘ

Ca+2↑, 2,   E-cadherin↑, 1,   MMP2↓, 1,   MMP3↓, 1,   MMP9↓, 1,   N-cadherin↓, 1,   PKCδ↓, 1,   SMAD3↓, 1,   p‑SMAD4↓, 1,   STAC2↓, 1,   TGF-β↓, 2,   TGF-β↑, 1,   TIMP1↑, 1,   TumCI↓, 2,   TumCMig↓, 2,   TumCP↓, 5,   Vim↓, 1,  

Angiogenesis & Vasculature ⓘ

angioG↓, 1,   eNOS↓, 1,   HIF-1↓, 1,   Hif1a↓, 2,   VEGF↓, 3,  

Barriers & Transport ⓘ

GLUT1↓, 1,  

Immune & Inflammatory Signaling ⓘ

CXCR4↓, 1,   p‑IKKα↓, 1,   JAK↓, 1,   JAK1↓, 1,   JAK2↓, 1,   NF-kB↓, 4,   TLR4↓, 1,  

Drug Metabolism & Resistance ⓘ

BioAv↓, 1,   ChemoSen↑, 4,   Dose↝, 1,   eff↑, 1,   eff↓, 1,   selectivity↑, 1,  

Clinical Biomarkers ⓘ

AFP↓, 1,   HER2/EBBR2↓, 2,  

Functional Outcomes ⓘ

cachexia↓, 1,   ChemoSideEff∅, 1,   OS↑, 1,  
Total Targets: 125

Pathway results for Effect on Normal Cells

Redox & Oxidative Stress ⓘ

ROS↑, 2,  

Mitochondria & Bioenergetics ⓘ

MMP↓, 2,  

Core Metabolism/Glycolysis ⓘ

PKM2↓, 1,  

Cell Death ⓘ

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

Synaptic & Neurotransmission ⓘ

p‑tau↓, 1,  

Protein Aggregation ⓘ

Aβ↓, 1,   BACE↓, 1,  

Drug Metabolism & Resistance ⓘ

BioAv↓, 1,  

Functional Outcomes ⓘ

cardioP↑, 1,   neuroP↑, 2,   toxicity↑, 1,  
Total Targets: 27

Research papers

Year Title Authors PMID Link Flag
2024Evaluating anticancer activity of emodin by enhancing antioxidant activities and affecting PKC/ADAMTS4 pathway in thioacetamide-induced hepatocellular carcinoma in ratsHanan M HassanPMC11168332https://pmc.ncbi.nlm.nih.gov/articles/PMC11168332/0
2023Emodin treatment of papillary thyroid cancer cell lines in vitro inhibits proliferation and enhances apoptosis via downregulation of NF‑κB and its upstream TLR4 signalingXin LiuPMC10623093https://pmc.ncbi.nlm.nih.gov/articles/PMC10623093/0
2023Anticancer action of naturally occurring emodin for the controlling of cervical cancerPriyanka S LandePMC10501891https://pmc.ncbi.nlm.nih.gov/articles/PMC10501891/0
2022Emodin Exhibits Strong Cytotoxic Effect in Cervical Cancer Cells by Activating Intrinsic Pathway of ApoptosisAmir Saeed—https://www.researchgate.net/publication/364966165_Emodin_Exhibits_Strong_Cytotoxic_Effect_in_Cervical_Cancer_Cells_by_Activating_Intrinsic_Pathway_of_Apoptosis0
2022Emodin exerts antitumor effects in ovarian cancer cell lines by preventing the development of cancer stem cells via epithelial mesenchymal transitionHeming LongPMC8822392https://pmc.ncbi.nlm.nih.gov/articles/PMC8822392/0
2022Emodin ameliorates antioxidant capacity and exerts neuroprotective effect via PKM2-mediated Nrf2 transactivationZhenjiang Ding—https://www.sciencedirect.com/science/article/abs/pii/S02786915210082310
2022The versatile emodin: A natural easily acquired anthraquinone possesses promising anticancer properties against a variety of cancersQing ZhangPMC9134920https://pubmed.ncbi.nlm.nih.gov/35637953/0
2021Emodin Induced Necroptosis and Inhibited Glycolysis in the Renal Cancer Cells by Enhancing ROSKe-jie WangPMC7837784https://pmc.ncbi.nlm.nih.gov/articles/PMC7837784/0
2021Emodin and emodin-rich rhubarb inhibits histone deacetylase (HDAC) activity and cardiac myocyte hypertrophyLevi W EvansPMC7162729https://pmc.ncbi.nlm.nih.gov/articles/PMC7162729/0
2021Is Emodin with Anticancer Effects Completely Innocent? Two Sides of the CoinEsra Küpeli AkkolPMC8198870https://pmc.ncbi.nlm.nih.gov/articles/PMC8198870/0
2020Emodin reduces Breast Cancer Lung Metastasis by suppressing Macrophage-induced Breast Cancer Cell Epithelial-mesenchymal transition and Cancer Stem Cell formationQing LiuPMC7381725https://pmc.ncbi.nlm.nih.gov/articles/PMC7381725/0
2020Traditional Chinese Medicine: Role in Reducing β-Amyloid, Apoptosis, Autophagy, Neuroinflammation, Oxidative Stress, and Mitochondrial Dysfunction of Alzheimer’s DiseaseShi-Yu ChenPMC7188934https://pmc.ncbi.nlm.nih.gov/articles/PMC7188934/0
2019Emodin enhances antitumor effect of paclitaxel on human non-small-cell lung cancer cells in vitro and in vivoShuifang ChenPMC6489594https://pmc.ncbi.nlm.nih.gov/articles/PMC6489594/0
2019Emodin inhibits colon cancer by altering BCL-2 family proteins and cell survival pathwaysIan T. Saunders—https://link.springer.com/article/10.1186/s12935-019-0820-30
2018Emodin Sensitizes Hepatocellular Carcinoma Cells to the Anti-Cancer Effect of Sorafenib through Suppression of Cholesterol MetabolismYoung-Seon KimPMC6213641https://pmc.ncbi.nlm.nih.gov/articles/PMC6213641/0
2018Anti-Cancer Effects of Emodin on HepG2 Cells as Revealed by 1H NMR Based Metabolic ProfilingYue-Xiao Xing29676152https://pubmed.ncbi.nlm.nih.gov/29676152/0
2017Induction of Apoptosis in HepaRG Cell Line by Aloe-Emodin through Generation of Reactive Oxygen Species and the Mitochondrial PathwayXiaoxv Dong28618413https://pubmed.ncbi.nlm.nih.gov/28618413/0
2017Emodin and rhein decrease levels of hypoxia-inducible factor-1α in human pancreatic cancer cells and attenuate cancer cachexia in athymic mice carrying these cellsLijuan HuPMC5675689https://pmc.ncbi.nlm.nih.gov/articles/PMC5675689/0
2017Aloe-emodin Induces Apoptosis in Human Liver HL-7702 Cells through Fas Death Pathway and the Mitochondrial Pathway by Generating Reactive Oxygen SpeciesXiaoxv Dong28444790https://pubmed.ncbi.nlm.nih.gov/28444790/0
2016Emodin Decreases Hepatic Hypoxia-Inducible Factor-1[Formula: see text] by Inhibiting its BiosynthesisFeifei Ma27430909https://pubmed.ncbi.nlm.nih.gov/27430909/0
2014Emodin inhibits LOVO colorectal cancer cell proliferation via the regulation of the Bcl-2/Bax ratio and cytochrome cLIANG MAPMC4151688https://pmc.ncbi.nlm.nih.gov/articles/PMC4151688/0
2013Emodin Isolated from Polygoni cuspidati Radix Inhibits TNF-α and IL-6 Release by Blockading NF-κB and MAP Kinase Pathways in Mast Cells Stimulated with PMA Plus A23187Yue LuPMC3879914https://pmc.ncbi.nlm.nih.gov/articles/PMC3879914/0
2013Emodin inhibits growth and induces apoptosis in an orthotopic hepatocellular carcinoma model by blocking activation of STAT3Aruljothi SubramaniamPMC3799595https://pmc.ncbi.nlm.nih.gov/articles/PMC3799595/0
2012Antitumor effects of emodin on LS1034 human colon cancer cells in vitro and in vivo: roles of apoptotic cell death and LS1034 tumor xenografts modelYi-Shih Ma22321733https://pubmed.ncbi.nlm.nih.gov/22321733/0
2010Aloe-emodin induces apoptosis of human nasopharyngeal carcinoma cells via caspase-8-mediated activation of the mitochondrial death pathwayMeng-Liang Lin19942342https://pubmed.ncbi.nlm.nih.gov/19942342/0
2009Aloe-emodin induces cell death through S-phase arrest and caspase-dependent pathways in human tongue squamous cancer SCC-4 cellsTsan-Hung Chiu20032398https://pubmed.ncbi.nlm.nih.gov/20032398/0
2009Emodin induces apoptosis of human tongue squamous cancer SCC-4 cells through reactive oxygen species and mitochondria-dependent pathwaysShuw-Yuan Lin19331169https://pubmed.ncbi.nlm.nih.gov/19331169/0
2009Emodin induces a reactive oxygen species-dependent and ATM-p53-Bax mediated cytotoxicity in lung cancer cellsJin-Mei Lai19744477https://pubmed.ncbi.nlm.nih.gov/19744477/0
2005Aloe emodin-induced apoptosis in t-HSC/Cl-6 cells involves a mitochondria-mediated pathwayLi-Hua Lian15910415https://pubmed.ncbi.nlm.nih.gov/15910415/0
2005Emodin induces apoptosis in human lung adenocarcinoma cells through a reactive oxygen species-dependent mitochondrial signaling pathwayYu-Ting Su15941563https://pubmed.ncbi.nlm.nih.gov/15941563/0