Snail Cancer Research Results

Snail, Snail: Click to Expand ⟱
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Snail gene may show a role in recurrence of breast cancer by downregulating E-cadherin and inducing an epithelial to mesenchymal transition. Snail promotes metastasis of breast cancer cells and overexpression of Snail is a biomarker of poor clinical outcome for patients with breast cancer.
Snail, a repressor of E-cadherin and an inducer of EMT.
Snail (SNAI1):
A transcription factor that plays a key role in the regulation of the epithelial-to-mesenchymal transition (EMT).
It suppresses the expression of epithelial markers (such as E-cadherin) and upregulates mesenchymal markers, facilitating changes in cell adhesion and motility.
EMT Induction:
Snail actively represses genes such as E-cadherin, a protein critical for cell–cell adhesion. Its upregulation leads to a loss of epithelial characteristics and the acquisition of a mesenchymal phenotype, enhancing migratory potential.
Invasion and Metastasis:
Through EMT induction, Snail facilitates tumor cell dissemination and invasion into surrounding tissues, thereby playing a central role in metastasis.

Elevated levels of Snail have been observed in a variety of cancers, including breast, colorectal, pancreatic, and head and neck cancers.
Elevated Snail expression is frequently associated with a worse prognosis, including lower overall survival rates and increased likelihood of metastasis.
Scientific Papers found: Click to Expand⟱
3383- ART/DHA,    Dihydroartemisinin: A Potential Natural Anticancer Drug
- Review, Var, NA
TumCP↓, DHA exerts anticancer effects through various molecular mechanisms, such as inhibiting proliferation, inducing apoptosis, inhibiting tumor metastasis and angiogenesis, promoting immune function, inducing autophagy and endoplasmic reticulum (ER) stres
Apoptosis↑,
TumMeta↓,
angioG↓,
TumAuto↑,
ER Stress↑,
ROS↑, DHA could increase the level of ROS in cells, thereby exerting a cytotoxic effect in cancer cells
Ca+2↑, activation of Ca2+ and p38 was also observed in DHA-induced apoptosis of PC14 lung cancer cells
p38↑,
HSP70/HSPA5↓, down-regulation of heat-shock protein 70 (HSP70) might participate in the apoptosis of PC3 prostate cancer cells induced by DHA
PPARγ↑, DHA inhibited the growth of colon tumor by inducing apoptosis and increasing the expression of peroxisome proliferator-activated receptor γ (PPARγ)
GLUT1↓, DHA was shown to inhibit the activity of glucose transporter-1 (GLUT1) and glycolytic pathway by inhibiting phosphatidyl-inositol-3-kinase (PI3K)/AKT pathway and downregulating the expression of hypoxia inducible factor-1α (HIF-1α)
Glycolysis↓, Inhibited glycolysis
PI3K↓,
Akt↓,
Hif1a↓,
PKM2↓, DHA could inhibit the expression of PKM2 as well as inhibit lactic acid production and glucose uptake, thereby promoting the apoptosis of esophageal cancer cells
lactateProd↓,
GlucoseCon↓,
EMT↓, regulating the EMT-related genes (Slug, ZEB1, ZEB2 and Twist)
Slug↓, Downregulated Slug, ZEB1, ZEB2 and Twist in mRNA level
Zeb1↓,
ZEB2↓,
Twist↓,
Snail?, downregulated the expression of Snail and PI3K/AKT signaling pathway, thereby inhibiting metastasis
CAFs/TAFs↓, DHA suppressed the activation of cancer-associated fibroblasts (CAFs) and mouse cancer-associated fibroblasts (L-929-CAFs) by inhibiting transforming growth factor-β (TGF-β signaling
TGF-β↓,
p‑STAT3↓, blocking the phosphorylation of STAT3 and polarization of M2 macrophages
M2 MC↓,
uPA↓, DHA could inhibit the growth and migration of breast cancer cells by inhibiting the expression of uPA
HH↓, via inhibiting the hedgehog signaling pathway
AXL↓, DHA acted as an Axl inhibitor in prostate cancer, blocking the expression of Axl through the miR-34a/miR-7/JARID2 pathway, thereby inhibiting the proliferation, migration and invasion of prostate cancer cells.
VEGFR2/KDR/Flk1↓, inhibition of VEGFR2-mediated angiogenesis
JNK↑, JNK pathway activated and Beclin 1 expression upregulated.
Beclin-1/ATG6↑,
GRP78/BiP↑, Glucose regulatory protein 78 (GRP78, an ER stress-related molecule) was upregulated after DHA treatment.
eff↑, results demonstrated that DHA-induced ER stress required iron
eff↑, DHA was used in combination with PDGFRα inhibitors (sunitinib and sorafenib), it could sensitize ovarian cancer cells to PDGFR inhibitors and achieved effective therapeutic efficacy
eff↑, DHA combined with 2DG (a glycolysis inhibitor) synergistically induced apoptosis through both exogenous and endogenous apoptotic pathways
eff↑, histone deacetylase inhibitors (HDACis) enhanced the anti-tumor effect of DHA by inducing apoptosis.
eff↑, DHA enhanced PDT-induced cell growth inhibition and apoptosis, increased the sensitivity of esophageal cancer cells to PDT by inhibiting the NF-κB/HIF-1α/VEGF pathway
eff↑, DHA was added to magnetic nanoparticles (MNP), and the MNP-DHA has shown an effect in the treatment of intractable breast cancer
IL4↓, downregulated IL-4;
DR5↑, Upregulated DR5 in protein, Increased DR5 promoter activity
Cyt‑c↑, Released cytochrome c from the mitochondria to the cytosol
Fas↑, Upregulated fas, FADD, Bax, cleaved-PARP
FADD↑,
cl‑PARP↑,
cycE/CCNE↓, Downregulated Bcl-2, Bcl-xL, procaspase-3, Cyclin E, CDK2 and CDK4
CDK2↓,
CDK4↓,
Mcl-1↓, Downregulated Mcl-1
Ki-67↓, Downregulated Ki-67 and Bcl-2
Bcl-2↓,
CDK6↓, Downregulated of Cyclin E, CDK2, CDK4 and CDK6
VEGF↓, Downregulated VEGF, COX-2 and MMP-9
COX2/PTGS2↓,
MMP9↓,

8105- KAE,    Chemo-preventive and therapeutic effect of the dietary flavonoid kaempferol: A comprehensive review
- Review, Var, NA
Apoptosis↑, It induces apoptosis (HeLa cervical cancer cells), decreases cell viability (G2/M phase), downregulates phosphoinositide 3-kinase (PI3K)/AKT
tumCV↓,
TumCCA↑,
PI3K↓,
Akt↓,
EMT↓, suppresses protein expression of epithelial-mesenchymal transition (EMT)-related markers including N-cadherin, E-cadherin, Slug, and Snail, and metastasis-related markers such as matrix metallopeptidase 2 (MMP-2).
N-cadherin↓,
E-cadherin↓, nhibition of N‐cadherin, E‐cadherin, Slug, Snail, and MMP‐2, 9, and cathepsin B, D
Slug?,
Snail?,
MMP2↓,
MMP9↓,
CTSB↓,
CTSD↓,
Casp3↑, Activation of caspase signals such as caspase‐3, ‐8, and ‐9
Casp8↑,
Casp9↑,
TIMP2↓, Down‐regulation of phosphorylated TIMP2, AKT, and MMP2 levels
Akt↓,
TumCD↑, Induction of cell apoptotic cell death, intracellular free calcium elevation, and mitochondrial membrane potential disruption.
i-Ca+2↑,
MMP↓,
*ROS↓, Enhances the concentrations of superoxide dismutase, catalase, glutathione peroxidase, and glutathione‐S‐transferase.
*SOD↑,
*Catalase↑,
*GPx↑,
*GSTs↑,
*AST↓, Lowers aspartate aminotransferase, alanine aminotransferase, malondialdehyde (MDA).
*ALAT↓,
*MDA↓,
*CYP2E1↓, Decreases activity of hepatic microsomal enzyme cytochrome 2E1 (CYP2E1) expression
*NRF2↑, Increases mRNA and protein expression of Nrf2‐regulated genes
*AGEs↓, Suppresses advanced glycation end products (AGEs)‐ receptor.
*IL6↓, Reduces levels of IL‐6, TNF‐α, and NF‐κB.
*TNF-α↓,
*NF-kB↓,
*Casp3↓, Lowers expressions of Caspase‐3 and Bax,
*BAX↓,
*antiAll↑, Antiallergic Inhibits COX2‐mediated production of prostaglandin D2 and prostaglandin F2α.
*COX2/PTGS2↓,
*PGE2↓,
*RUNX2↑, Increases expression of the osteoblast‐activated factors RUNX‐2, BMP‐2, osterix, collagen I, and SQSTM1/p62
*BMP2↑,
*COL1↑,
*p62↑,
*FASN↓, Reduces expressions of lipin1, FASN, LPAATθ (lysophosphatidic acid acyltransferase), SREBP‐1C (fatty acid synthetic proteins), and DGAT1 (triglyceride synthetic enzymes).
*DGAT1↓,
FOXP3↑, kaempferol significantly enhanced the inhibitory effect of proliferation, increased the FOXP3 expression level,
DNAdam↑, s induction of DNA damage, enhancement DNA condensation
ROS↑, anti‐cancer property is mainly defined by ROS accumulation due to catalase inhibition as depicted in Figure 2
Catalase↓,
*ROS↓, (A/R)‐induced injury of cardiomyocytes by increasing cell viability, lowering LDH release, reducing A/R‐induced ROS generation, loss of Δψm, and release of cytochrome c from mitochondria into cytosol.
*MMP↑,
*Cyt‑c↓,


Showing Research Papers: 1 to 2 of 2

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 2

Pathway results for Effect on Cancer / Diseased Cells:


Redox & Oxidative Stress(tgid=1) ⓘ

Catalase↓, 1,   ROS↑, 2,  

Mitochondria & Bioenergetics(tgid=3) ⓘ

MMP↓, 1,  

Core Metabolism/Glycolysis(tgid=4) ⓘ

GlucoseCon↓, 1,   Glycolysis↓, 1,   lactateProd↓, 1,   PKM2↓, 1,   PPARγ↑, 1,  

Cell Death(tgid=5) ⓘ

Akt↓, 3,   Apoptosis↑, 2,   Bcl-2↓, 1,   Casp3↑, 1,   Casp8↑, 1,   Casp9↑, 1,   Cyt‑c↑, 1,   DR5↑, 1,   FADD↑, 1,   Fas↑, 1,   JNK↑, 1,   Mcl-1↓, 1,   p38↑, 1,   TumCD↑, 1,  

Transcription & Epigenetics(tgid=7) ⓘ

tumCV↓, 1,  

Protein Folding & ER Stress(tgid=8) ⓘ

ER Stress↑, 1,   GRP78/BiP↑, 1,   HSP70/HSPA5↓, 1,  

Autophagy & Lysosomes(tgid=9) ⓘ

Beclin-1/ATG6↑, 1,   TumAuto↑, 1,  

DNA Damage & Repair(tgid=10) ⓘ

DNAdam↑, 1,   cl‑PARP↑, 1,  

Cell Cycle & Senescence(tgid=11) ⓘ

CDK2↓, 1,   CDK4↓, 1,   cycE/CCNE↓, 1,   TumCCA↑, 1,  

Proliferation, Differentiation & Cell State(tgid=12) ⓘ

CTSB↓, 1,   CTSD↓, 1,   EMT↓, 2,   HH↓, 1,   PI3K↓, 2,   p‑STAT3↓, 1,  

Migration(tgid=13) ⓘ

AXL↓, 1,   Ca+2↑, 1,   i-Ca+2↑, 1,   CAFs/TAFs↓, 1,   E-cadherin↓, 1,   Ki-67↓, 1,   MMP2↓, 1,   MMP9↓, 2,   N-cadherin↓, 1,   Slug?, 1,   Slug↓, 1,   Snail?, 2,   TGF-β↓, 1,   TIMP2↓, 1,   TumCP↓, 1,   TumMeta↓, 1,   Twist↓, 1,   uPA↓, 1,   Zeb1↓, 1,   ZEB2↓, 1,  

Angiogenesis & Vasculature(tgid=14) ⓘ

angioG↓, 1,   Hif1a↓, 1,   VEGF↓, 1,   VEGFR2/KDR/Flk1↓, 1,  

Barriers & Transport(tgid=15) ⓘ

GLUT1↓, 1,  

Immune & Inflammatory Signaling(tgid=16) ⓘ

COX2/PTGS2↓, 1,   FOXP3↑, 1,   IL4↓, 1,   M2 MC↓, 1,  

Hormonal & Nuclear Receptors(tgid=20) ⓘ

CDK6↓, 1,  

Drug Metabolism & Resistance(tgid=21) ⓘ

eff↑, 6,  

Clinical Biomarkers(tgid=22) ⓘ

Ki-67↓, 1,  
Total Targets: 72

Pathway results for Effect on Normal Cells:


NA, unassigned(tgid=0) ⓘ

antiAll↑, 1,  

Redox & Oxidative Stress(tgid=1) ⓘ

Catalase↑, 1,   CYP2E1↓, 1,   GPx↑, 1,   GSTs↑, 1,   MDA↓, 1,   NRF2↑, 1,   ROS↓, 2,   SOD↑, 1,  

Mitochondria & Bioenergetics(tgid=3) ⓘ

MMP↑, 1,  

Core Metabolism/Glycolysis(tgid=4) ⓘ

ALAT↓, 1,   DGAT1↓, 1,   FASN↓, 1,  

Cell Death(tgid=5) ⓘ

BAX↓, 1,   BMP2↑, 1,   Casp3↓, 1,   Cyt‑c↓, 1,  

Autophagy & Lysosomes(tgid=9) ⓘ

p62↑, 1,  

Proliferation, Differentiation & Cell State(tgid=12) ⓘ

RUNX2↑, 1,  

Migration(tgid=13) ⓘ

COL1↑, 1,  

Immune & Inflammatory Signaling(tgid=16) ⓘ

COX2/PTGS2↓, 1,   IL6↓, 1,   NF-kB↓, 1,   PGE2↓, 1,   TNF-α↓, 1,  

Protein Aggregation(tgid=19) ⓘ

AGEs↓, 1,  

Clinical Biomarkers(tgid=22) ⓘ

ALAT↓, 1,   AST↓, 1,   IL6↓, 1,  
Total Targets: 29

Scientific Paper Hit Count for: Snail, Snail
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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