EpCAM Cancer Research Results

EpCAM, epithelial Cell Adhesion Molecule: Click to Expand ⟱
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EpCAM (Epithelial Cell Adhesion Molecule) is a cell surface protein that plays a significant role in cell adhesion, proliferation, and differentiation. It is primarily expressed in epithelial tissues and is involved in various cellular processes, including the maintenance of tissue architecture and the regulation of cell signaling.
EpCAM is often overexpressed in various types of cancers, including breast, colorectal, prostate, and lung cancers.
Scientific Papers found: Click to Expand⟱
4675- CUR,    Curcumin improves the efficacy of cisplatin by targeting cancer stem-like cells through p21 and cyclin D1-mediated tumour cell inhibition in non-small cell lung cancer cell lines
- in-vitro, NSCLC, A549
ChemoSen↑, we showed that curcumin enhanced the sensitivity of the double-positive (CD166+/EpCAM+) CSC subpopulation in non-small cell lung cancer (NSCLC) cell lines (A549 and H2170) to cisplatin-induced apoptosis and inhibition of metastasis.
CSCs↓, Curcumin enhances the sensitivity of the CSC subpopulation of CD166+/EpCAM+ cells to cisplatin-induced apoptosis
EpCAM↓, curcumin enhanced the inhibitory effects of cisplatin on the highly migratory CD166+/EpCAM+ subpopulation
TumCCA↓, combined treatments induced cell cycle arrest, therefore triggering CSC growth inhibition via the intrinsic apoptotic pathway.
VEGF↓, curcumin markedly decreased the metastasis of breast tumour cells to the lung and suppressed the expression of vascular endothelial growth factor (VEGF), matrix metalloproteinase-9 (MMP-9)
MMP9↓,
toxicity↓, Furthermore, curcumin has been found to be safe when administered at ≤10 g/day in humans

431- CUR,    Curcumin suppresses the stemness of non-small cell lung cancer cells via promoting the nuclear-cytoplasm translocation of TAZ
- in-vitro, Lung, A549 - in-vitro, Lung, H1299
ALDH1A1↓,
CD133↓,
EpCAM↓,
OCT4↓,
TAZ↓,
Hippo↑,
p‑TAZ↑,

6325- Eug,    Anticancer Properties of Eugenol: A Review
- Review, Var, NA
*antiOx↑, long been utilized all over the world as a result of its broad properties like antioxidant, anticancer, anti-inflammatory, and antimicrobial activities. Both eugenol and clove oil display potent antioxidant capabilities.
*AntiCan↑,
*Inflam↓, Eugenol Anti-Inflammatory Agent
TumCD↑, Anticancer effects of eugenol are accomplished by various mechanisms like inducing cell death, cell cycle arrest, inhibition of migration, metastasis, and angiogenesis on several cancer cell lines.
TumCCA↑,
TumCMig↓,
TumMeta↓,
angioG↓,
ChemoSen↑, eugenol might be utilized as an adjunct remedy for patients who are treated with conventional chemotherapy. This combination leads to a boosted effectiveness with decreased toxicity.
chemoP↑,
*BioAv↝, Eugenol is an aromatic pale yellowish liquid that dissolves well in organic solvents and moderately in water.
*BioAv↑, Eugenol is susceptible to oxidation and many biochemical interactions. It is quickly absorbed via diverse organs and processed in the liver when taken orally.
*BioAv↑, encapsulation of eugenol appears to be the finest approach for avoiding early absorption, improving its water solubility, and, therefore, increasing its action.
*BioAv↑, when eugenol is supplied as solid lipid nanoparticles, the quantity of eugenol delivered to infected cells upsurges by at least sixfold
*Bacteria↓, Eugenol is well-known for its antibacterial properties.
*ROS↓, They possess a potent DPPH radical scavenging influence (half maximal inhibitory concentration (IC50) = 11.7 μg/mL for eugenol; 13.2 μg/mL for clove oil) and hinder reactive oxygen species (ROS) generation in human neutrophils
*IL6↓, exposure of rats to eugenol (10.7 mg/kg body weight/day) for 15 days reduced the translation of inflammatory markers (IL-6, COX-2, and TNF-α), lipid peroxidation indices, and protein oxidation [51].
*COX2↓,
*TNF-α↓,
*lipid-P↓,
*SOD1↑, Pretreatment with eugenol was capable of dramatically enhancing SOD1, CAT, Gpx1, and GST levels as well as decreasing inflammation triggered via lung exposure to LPS.
*Catalase↑,
*GPx1↑,
*GSTs↑,
ROS↑, Eugenol triggered cell apoptosis in these cancerous cells through a process reliant on elevated ROS production and decreased the mitochondrial membrane potential, indicating that it might possess apoptosis-triggering characteristics
MMP↓,
Apoptosis↑,
COX2↓, Lung cancer in vitro low concentrations to 1000 μM reduces cyclooxygenase-2 activity, promotes cell cycle arrest at S-phase
TumCCA↑,
E2Fs↓, Breast cancer in vitro and in vivo 2 µM down regulating E2F1
PI3K↓, inhibition of the PI3K/Akt pathway and prevention of MMP (matrix metalloproteinase) action, an in-laboratory study using lung cancer
Akt↓,
MMPs↓,
CSCs↓, CSC markers like Oct4, CD44, EpCAM, and Notcht1, whose expression is reliant on β-catenin, were considerably reduced,
OCT4↓,
CD44↓,
EpCAM↓,
NOTCH1↓,
TumVol↓, Eugenol works through the synthesis of ROS [82], which leads to DNA synthesis inhibition, hence postponing cancer progress. A 40% decrease was documented in tumor size via eugenol activity
Casp3↑, Elevated caspase-3, p53, and PARP cleavage levels are associated with eugenol-triggered apoptosis in HOS cells
P53↑,
cl‑PARP↑,
MMP2↓, Eugenol-treated cells demonstrated substantially reduced expression of MMP2 and MMP9 and an insignificant rise in the expression of TIMP1 in HER2-positive and triple-negative breast cancer cells.
MMP9↓,
TIMP1↑,
ALDH↓, Eugenol is thought to help cisplatin suppress breast cancer stem cells by hindering the action of aldehyde dehydrogenases (ALDH) and ALDH-positive cancer beginning cells, as well as inhibiting the NF-B signaling pathway.
NF-kB↓,
*toxicity↓, Overall, the toxic effect of eugenol on mammals is low, and the US Environmental Protection Agency has categorized eugenol as category 3. The oral LD50 value is >1930 mg kg−1 in rodents

6330- Eug,    Molecular Mechanisms of Action of Eugenol in Cancer: Recent Trends and Advancement
- Review, Var, NA
TumCD↑, investigations reveal eugenol inducing cytotoxicity, inhibiting phases of the cell cycles, programmed cell death, and auto-phagocytosis in studied cancer lines; thus, portraying eugenol as a promising anticancer molecule.
TumCCA↑,
AntiCan↑,
Apoptosis↑, The suggested techniques can be enlisted as induction of apoptosis, cell cycle arrest, reducing angiogenesis, interplaying dual roles as an oxidant and pro-oxidant, inhibiting inflammation, and stopping cellular invasion and metastasis.
angioG↓,
TumCI↓,
TumMeta↓,
ChemoSen↑, Combining cisplatin (30 µM) with eugenol (1 µM) potentiated its chemotherapeutic activity by inhibiting aldehyde dehydrogenases (ALDH) enzyme activity, impeding the nuclear factor kappa B (NF-κB) and signaling cascade by reducing binding affinity of
ALDH↓,
NF-kB↓,
IL6↓, downregulating IL-6 and IL-8 mRNA (messenger ribonucleic acid).
IL8↓,
BAX↑, Increased Bcl-2/Bax ratio, elevated levels of proapoptotic protein Bax, increased expression of cleaved caspases-3 and -9, cleaved poly (ADP-ribose) polymerase (PARP) on the higher side
cl‑Casp3↑,
cl‑Casp9↑,
cl‑PARP↑,
Bcl-2↓, epression of anti-apoptotic protein B-cell lymphoma 2 (Bcl-2) accounted for the apoptotic potential for the combination of eugenol and cisplatin.
MMP2↓, repression of the expression level of matrix metalloproteinase-2 (MMP-2) and matrix metalloproteinase-9 (MMP-9) explained the inhibition of the invasive tendency of the TNBCs by combination therapy
MMP9↓,
EMT↓, Reduced epithelial-to-mesenchymal transition (EMT) was evident from reduced expressions of N-cadherin and Snail1 and higher E-cadherin expression.
N-cadherin↓,
Snail↓,
E-cadherin↑,
SOX2↓, Inhibition of pluripotency was evident by reduced expression of biomarker Sox-2 [(sex determining region Y)-box 2]
ROS↑, (MCF-7) (IC50: 22.75 𝜇M) and MDA-MB-231 (IC50: 15.09 𝜇M) breast cancer cells with increasing ROS levels which inhibited cell cycle at G2/M phase, that leads to clastogenesis in vitro.
PCNA↓, downregulated the proliferation of the cell nuclear antigen (PCNA) associated with deceased mitochondria membrane potential (ΔΨm) and upregulation of Bcl-2 associated X protein (Bax)
MMP1↓,
Cyt‑c↑, release of cytochrome-c and lactate dehydrogenase was also observed at a concentration of eugenol of more than 0.9 mM.
LDH↑,
CSCs↓, Downregulation of cancer stem cell markers octamer-binding transcription factor 4 (oct4), Notch1 (Neurogenic locus notch homolog protein 1), epithelial cellular adhesion molecule (EpCAM), and CD44 was observed in the stem cells
OCT4↓,
NOTCH1↓,
EpCAM↓,
CD44↓,
HER2/EBBR2↓, A therapeutic dose (80 μM) of eugenol was shown to cease the proliferating of human epidermal growth factor of receptor 2 (HER-2) positive MCF-10AT cell lines by 32.8%.
VEGF↓, The expression of vascular endothelial growth factor (VEGF), vascular endothelial growth factor receptor 1 (VEGFR1), and MMPs are all reduced by eugenol, while that of reversion-inducing-cysteine-rich protein with kazal motifs (RECK) and TIMP-2 is in
TIMP2↑,
eff↑, Eugenol-loaded chitosan nanopolymers (IC50: 7.5 µM) convincingly induce apoptosis and inhibition of metastasis in rat C6 glioma cells.
Ca+2↑, Eugenol (100–300 µM) stimulated PLC-dependent Ca2+ discharge from the endoplasmic reticulum and promoted Ca2+ influx
TumVol↓, Eugenol significantly reduced tumors (nearly 40%) and delayed the time to the endpoint (by 19%) in B16 melanoma xenografts.
DNAdam↑, EUG MCF-7 cells ↑ DNA fragmentation, ↓ intracellular glutathione level, ↑ intracellular H2O2 and lipid peroxidation, ↑ apoptosis 1–4 mM
GSH↓,
H2O2↑,
lipid-P↑,

59- QC,    Quercetin Inhibits Breast Cancer Stem Cells via Downregulation of Aldehyde Dehydrogenase 1A1 (ALDH1A1), Chemokine Receptor Type 4 (CXCR4), Mucin 1 (MUC1), and Epithelial Cell Adhesion Molecule (EpCAM)
- in-vitro, BC, MDA-MB-231
ALDH1A1↓, lowered the expression levels of proteins related to tumorigenesis and cancer progression, such as aldehyde dehydrogenase 1A1, C-X-C chemokine receptor type 4, mucin 1, and epithelial cell adhesion molecules.
CXCR4↓,
MUC1↓,
EpCAM↓,
CSCs↓, quercetin suppressed breast cancer stem cell proliferation, self-renewal, and invasiveness
TumCP↓,
TumCI↓,
CD44↓, High doses of quercetin inhibit proliferation of MDA-MB-231 cells and CD44+/CD24− CSCs
CD24↓,
Apoptosis↑, Quercetin induces apoptosis of MDA-MB-231 cells
TumCCA↑, These results indicate that quercetin alters the MDA-MB-231 cell cycle

96- QC,  docx,    Quercetin reverses docetaxel resistance in prostate cancer via androgen receptor and PI3K/Akt signaling pathways
- vitro+vivo, Pca, LNCaP - in-vitro, Pca, PC3
PI3K/Akt↓, PI3K/Akt signaling pathway was excessively activated after prostate cancer cells developed resistance to docetaxel. And quercetin could also reverse the activation of this pathway.
Ki-67↓,
BAX↑,
Bcl-2↓,
EpCAM↓,
Twist↓, Twist2
E-cadherin↑,
P-gp↓, Quercetin reverses docetaxel resistance by reversing the up-regulation of P-gp
TumCP↓, quercetin had the reversal effect of docetaxel-resistance, which could inhibit cell proliferation, migration, invasion and colony formation of docetaxel-resistant prostate cancer cells.
TumCMig↓,
TumCI↓,

631- VitC,    Vitamin C preferentially kills cancer stem cells in hepatocellular carcinoma via SVCT-2
- vitro+vivo, Liver, NA
SVCT-2∅, response to VC was correlated with sodium-dependent vitamin C transporter 2 (SVCT-2) expressions. Most importantly, SVCT-2 was highly expressed in liver CSCs
ROS↑,
DNAdam↑,
ATP↓,
TumCCA↑,
Apoptosis↑,
OS↑, VC use was linked to improved disease-free survival (DFS) in HCC patients
CD133↓, CD133+
EpCAM↓, EpCAM+
OV6↓, OV6+
γH2AX↑, p-H2AX induced by VC


Showing Research Papers: 1 to 7 of 7

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 7

Pathway results for Effect on Cancer / Diseased Cells:


Redox & Oxidative Stress ⓘ

GSH↓, 1,   H2O2↑, 1,   lipid-P↑, 1,   ROS↑, 3,  

Mitochondria & Bioenergetics ⓘ

ATP↓, 1,   MMP↓, 1,  

Core Metabolism/Glycolysis ⓘ

LDH↑, 1,   PI3K/Akt↓, 1,  

Cell Death ⓘ

Akt↓, 1,   Apoptosis↑, 4,   BAX↑, 2,   Bcl-2↓, 2,   Casp3↑, 1,   cl‑Casp3↑, 1,   cl‑Casp9↑, 1,   Cyt‑c↑, 1,   Hippo↑, 1,   TumCD↑, 2,  

Kinase & Signal Transduction ⓘ

HER2/EBBR2↓, 1,  

Transcription & Epigenetics ⓘ

OV6↓, 1,  

DNA Damage & Repair ⓘ

DNAdam↑, 2,   P53↑, 1,   cl‑PARP↑, 2,   PCNA↓, 1,   γH2AX↑, 1,  

Cell Cycle & Senescence ⓘ

E2Fs↓, 1,   TumCCA↓, 1,   TumCCA↑, 5,  

Proliferation, Differentiation & Cell State ⓘ

ALDH↓, 2,   ALDH1A1↓, 2,   CD133↓, 2,   CD24↓, 1,   CD44↓, 3,   CSCs↓, 4,   EMT↓, 1,   EpCAM↓, 7,   NOTCH1↓, 2,   OCT4↓, 3,   PI3K↓, 1,   SOX2↓, 1,   TAZ↓, 1,   p‑TAZ↑, 1,  

Migration ⓘ

Ca+2↑, 1,   E-cadherin↑, 2,   Ki-67↓, 1,   MMP1↓, 1,   MMP2↓, 2,   MMP9↓, 3,   MMPs↓, 1,   MUC1↓, 1,   N-cadherin↓, 1,   Snail↓, 1,   TIMP1↑, 1,   TIMP2↑, 1,   TumCI↓, 3,   TumCMig↓, 2,   TumCP↓, 2,   TumMeta↓, 2,   Twist↓, 1,  

Angiogenesis & Vasculature ⓘ

angioG↓, 2,   VEGF↓, 2,  

Barriers & Transport ⓘ

P-gp↓, 1,   SVCT-2∅, 1,  

Immune & Inflammatory Signaling ⓘ

COX2↓, 1,   CXCR4↓, 1,   IL6↓, 1,   IL8↓, 1,   NF-kB↓, 2,  

Drug Metabolism & Resistance ⓘ

ChemoSen↑, 3,   eff↑, 1,  

Clinical Biomarkers ⓘ

HER2/EBBR2↓, 1,   IL6↓, 1,   Ki-67↓, 1,   LDH↑, 1,  

Functional Outcomes ⓘ

AntiCan↑, 1,   chemoP↑, 1,   OS↑, 1,   toxicity↓, 1,   TumVol↓, 2,  
Total Targets: 79

Pathway results for Effect on Normal Cells:


Redox & Oxidative Stress ⓘ

antiOx↑, 1,   Catalase↑, 1,   GPx1↑, 1,   GSTs↑, 1,   lipid-P↓, 1,   ROS↓, 1,   SOD1↑, 1,  

Immune & Inflammatory Signaling ⓘ

COX2↓, 1,   IL6↓, 1,   Inflam↓, 1,   TNF-α↓, 1,  

Drug Metabolism & Resistance ⓘ

BioAv↑, 3,   BioAv↝, 1,  

Clinical Biomarkers ⓘ

IL6↓, 1,  

Functional Outcomes ⓘ

AntiCan↑, 1,   toxicity↓, 1,  

Infection & Microbiome ⓘ

Bacteria↓, 1,  
Total Targets: 17

Scientific Paper Hit Count for: EpCAM, epithelial Cell Adhesion Molecule
2 Curcumin
2 Eugenol
2 Quercetin
1 Docetaxel
1 Vitamin C (Ascorbic Acid)
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

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