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)
Scientific Papers found: Click to Expand⟱
1323- EMD,    Anticancer action of naturally occurring emodin for the controlling of cervical cancer
- Review, Cerv, NA
TumCCA↑, cell cycle arrest in the G2/M phase
DNAdam↑,
mTOR↓,
Casp3↑,
Casp8↑,
Casp9↑,
TGF-β↑,
SMAD3↓,
p‑SMAD4↓,
ROS↑,
MMP↓,
CXCR4↓,
HER2/EBBR2↓,
ER Stress↓,
TumAuto↑, can increase the level of autophagy in A549 lung cancer cells, but did not affect autophagy in healthy non-cancerous Ha CaT cells
NOTCH1↓,

2422- EMD,    Anti-Cancer Effects of Emodin on HepG2 Cells as Revealed by 1H NMR Based Metabolic Profiling
- in-vitro, HCC, HepG2
HK2↓, The mRNA levels of hexokinase II (HKII), pyruvate kinase isoform M2 (PKM2) and lactate 19 dehydrogenase-A (LDHA) in emodin treated cells were all decreased in a concentration-dependent manner
PKM2↓,
LDHA↓,
Glycolysis↓, levels of glycolysis related proteins were significantly decreased. emodin indeed inhibited glycolysis of HepG2 cells.
TumCCA↑, induced cell cycle arrest, apoptosis and ROS generation
ROS↓,
glut↓, level of glutamine was decreased after emodin treatment
Hif1a↓, generation of ROS induces decreased expression of HIF-1

2345- EMD,    Emodin ameliorates antioxidant capacity and exerts neuroprotective effect via PKM2-mediated Nrf2 transactivation
- in-vitro, AD, PC12
*PKM2↓, Notably, emodin at nontoxic concentrations significantly inhibits PKM2 activity and promotes dissociation of tetrameric PKM2 into dimers in cells
*neuroP↑, emodin is a potential candidate for the treatment of oxidative stress-related neurodegenerative disorders

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↑, S-phase cell cycle arrest
*P21↑,
*cycE↑,
*cycA1↓,
*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↑, induced G(2)/M phase arrest
CycB↑,
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, NA
tumCV↓,
Casp3↑,
Casp9↑,
MMP↓,
Cyt‑c↑, cytochrome c increased in the cytosol but decreased in the mitochondria
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
TumCCA↑, S-phase arrest
eff↓, The free radical scavenger N-acetylcysteine (NAC) and caspase inhibitors markedly blocked aloe-emodin-induced apoptosis
P53↑,
P21↑,
p27↑,
cycA1↓,
cycE↓,
TS↓,
CDC25↓, Cdc25A
AIF↑, promoted the release of apoptosis-inducing factor (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↑, G2/M arrest
P21↑,
Chk2↑,
CycB↓,
cDC2↓,
Apoptosis↑,
Cyt‑c↑, release of cytochrome c from mitochondria
Casp9↑,
Casp3↑,
ROS↑,
MMP↓,
Bax:Bcl2↑,
ER Stress↑,

1327- EMD,    Emodin induces apoptosis in human lung adenocarcinoma cells through a reactive oxygen species-dependent mitochondrial signaling pathway
- in-vitro, Lung, A549
Cyt‑c↑, pronounced release of cytochrome c
Casp2↑,
Casp3↑,
Casp9↑,
ERK↓,
Akt↓,
ROS↑, free radical scavenger ascorbic acid and N-acetylcysteine attenuated emodin-mediated ROS production, ERK and AKT inactivation, mitochondrial dysfunction, Bcl-2/Bax modulation, and apoptosis
MMP↓,
Bcl-2↓,
BAX↑,

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↑,

1325- EMD,  PacT,    Emodin enhances antitumor effect of paclitaxel on human non-small-cell lung cancer cells in vitro and in vivo
- vitro+vivo, Lung, A549
TumCP↓,
Apoptosis↑,
BAX↑,
Casp3↑,
Bcl-2↓, decreasing the levels of Bcl-2, p-Akt and p-ERK
p‑Akt↓,
p‑ERK↓,
ChemoSideEff∅, without significant side effects in vivo.
ChemoSen↑, Combination of emodin with PTX synergistically inhibited the proliferation of A549 cells in vitro

1324- EMD,    Is Emodin with Anticancer Effects Completely Innocent? Two Sides of the Coin
- Review, Var, NA
*toxicity↑, however, it is known that emodin, which shows toxicity to cancer cells, may cause kidney toxicity, hepatotoxicity, and reproductive toxicity especially at high doses and long-term use.
*BioAv↓, poor oral bioavailability
Akt↓,
ERK↓,
ROS↑, pretreatment of cells with ascorbic acid prevented the induction of ROS by emodin and inhibited the upregulation of p53
MMP↓,
Bcl-2↓,
BAX↑,
TumCCA↑, increasing the percentage of both S and G2/M phase cells

950- EMD,    Emodin Decreases Hepatic Hypoxia-Inducible Factor-1[Formula: see text] by Inhibiting its Biosynthesis
- in-vivo, NA, NA - in-vitro, Liver, HepG2
HIF-1↓, emodin inhibited obesity-induced HIF-1 (liver and muscle, not kidney or in fat)

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↑, DOX combined with emodin can improve the sensitivity of MDA-MB-231 and MCF-7 cells to chemotherapy
eff↑, emodin was reported to increase the anti-proliferative effect of an EGFR inhibitor (afatinib) against PC through downregulation of EGFR by promoting STAT3
ChemoSen↑, gemcitabine combined with emodin increased cell death
angioG↓,
VEGF↓,
MMP2↓,
eNOS↓,
FOXD3↑,
MMP9↓,
TIMP1↑,

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, NA
tumCV↓,
TumCCA↑, induced G2/M phase arrest
ROS↑,
Ca+2↑,
MMP↓,
Apoptosis↑,
Cyt‑c↑,
Casp9↑,
Bax:Bcl2↑,

1320- EMD,  SRF,    Emodin Sensitizes Hepatocellular Carcinoma Cells to the Anti-Cancer Effect of Sorafenib through Suppression of Cholesterol Metabolism
- vitro+vivo, HCC, HepG2 - in-vitro, HCC, Hep3B - in-vitro, HCC, HUH7 - vitro+vivo, Hepat, SK-HEP-1
SREBF2↓,
Akt↓,
TumCCA↑, increased cell cycle arrest in the G1 phase
TumCG↓, combination of emodin and sorafenib was sufficient to inhibit tumor growth.
STAT3↓,

1319- EMD,    Emodin treatment of papillary thyroid cancer cell lines in vitro inhibits proliferation and enhances apoptosis via downregulation of NF‑κB and its upstream TLR4 signaling
- in-vitro, Thyroid, TPC-1 - in-vitro, Thyroid, IHH4
NF-kB↓,
TLR4↓,
TumCI↓,
TumCMig↓,

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↑, induced S and G2/M phase cell cycle arrest
*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↑, cytochrome c was released from the mitochondria to the cytoplasm

1247- EMD,    Emodin exerts antitumor effects in ovarian cancer cell lines by preventing the development of cancer stem cells via epithelial mesenchymal transition
- vitro+vivo, Ovarian, SKOV3 - in-vitro, Ovarian, A2780S
TumCP↓,
TumCMig↓,
TumCI↓,
EMT↓,
N-cadherin↓,
Vim↓,
E-cadherin↑,
TumCG↓, vivo
CD133↓,
OCT4↓,
CSCs↓,

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↓, Emodin suppressed TGF-β1 production in breast cancer cells
EMT↓,
CSCs↓,

1245- EMD,    Emodin Exhibits Strong Cytotoxic Effect in Cervical Cancer Cells by Activating Intrinsic Pathway of Apoptosis
- in-vitro, Cerv, HeLa
TumCG↓, emodin strongly inhibited the HeLa cell growth and proliferatio
TumCP↓,
Apoptosis↑,
ROS↑, observed significant ROS generation and caspases activation
Casp3↑,
Casp9↑,
MMP↓,
DNAdam↑,
GSH↓,

988- EMD,    Emodin Induced Necroptosis and Inhibited Glycolysis in the Renal Cancer Cells by Enhancing ROS
- in-vitro, RCC, NA
Necroptosis↑, emodin induces necroptosis, but not apoptosis, in renal cancer cells
p‑RIP1↑,
MLKL↑,
ROS↑, levels of ROS increased upon emodin treatment in a dose-dependent manner
Glycolysis↓,
GLUT1↓,
PI3K↓,
Akt↓,


* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 23

Results for Effect on Cancer/Diseased Cells:
AIF↑,1,   Akt↓,5,   p‑Akt↓,1,   angioG↓,1,   Apoptosis↑,6,   ATM↑,1,   ATP↓,1,   BAX↑,6,   Bax:Bcl2↑,4,   Bcl-2↓,4,   Ca+2↑,2,   Casp2↑,1,   Casp3↑,8,   Casp8↑,1,   Casp9↑,7,   proCasp9↓,1,   CD133↓,1,   cDC2↓,1,   CDC25↓,1,   ChemoSen↑,3,   ChemoSideEff∅,1,   Chk2↑,1,   CSCs↓,2,   CXCR4↓,1,   cycA1↓,1,   CycB↓,1,   CycB↑,1,   cycE↓,1,   CYP1A1↑,1,   Cyt‑c↑,6,   DNAdam↑,4,   E-cadherin↑,1,   eff↓,1,   eff↑,1,   EMT↓,3,   eNOS↓,1,   ER Stress↓,1,   ER Stress↑,2,   ERK↓,2,   p‑ERK↓,1,   FASN↓,1,   FOXD3↑,1,   glut↓,1,   GLUT1↓,1,   Glycolysis↓,2,   GSH↓,1,   HER2/EBBR2↓,2,   HIF-1↓,1,   Hif1a↓,1,   HK2↓,1,   JAK↓,1,   LDHA↓,1,   MAPK↓,1,   MLKL↑,1,   MMP↓,10,   MMP2↓,1,   MMP9↓,1,   mTOR↓,1,   N-cadherin↓,1,   Necroptosis↑,1,   NF-kB↓,2,   NOTCH1↓,1,   OCT4↓,1,   P21↑,2,   p27↑,1,   P53↑,2,   cl‑PARP↑,1,   PI3K↓,2,   PKM2↓,1,   p‑RIP1↑,1,   ROS↓,1,   ROS↑,10,   SMAD3↓,1,   p‑SMAD4↓,1,   SREBF2↓,1,   STAC2↓,1,   STAT3↓,1,   TGF-β↓,2,   TGF-β↑,1,   TIMP1↑,1,   TLR4↓,1,   TS↓,1,   TumAuto↑,2,   TumCCA↑,9,   TumCG↓,3,   TumCI↓,2,   TumCMig↓,2,   TumCP↓,4,   tumCV↓,2,   VEGF↓,1,   Vim↓,1,  
Total Targets: 91

Results for Effect on Normal Cells:
Bax:Bcl2↑,2,   BioAv↓,1,   Casp3↑,1,   cl‑Casp3↑,1,   Casp8↑,1,   cl‑Casp8↑,1,   Casp9↑,1,   cl‑Casp9↑,1,   CDK2↓,1,   cycA1↓,1,   cycE↑,1,   Fas↑,2,   MMP↓,2,   neuroP↑,1,   P21↓,1,   P21↑,2,   P53↑,2,   cl‑PARP↑,2,   PKM2↓,1,   ROS↑,2,   toxicity↑,1,   TumCCA↑,2,   tumCV↓,1,  
Total Targets: 23

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