Slug Cancer Research Results

Slug, transcription factor Slug: Click to Expand ⟱
Source:
Type:
Slug is well known to promote tumor progression and metastasis through the epithelial-mesenchymal transition (EMT), causing loss of cell adhesion and polarity while conferring migratory and invasive properties.
Slug/SNAI2: A transcription factor that belongs to the Snail family. It is best known for its role in regulating epithelial-to-mesenchymal transition (EMT).
Expression: Upregulation of Slug in cancers is often associated with the induction of EMT. This causes cells to lose epithelial markers (like E-cadherin) and gain mesenchymal markers, leading to increased invasiveness.
Metastatic Spread: By promoting EMT, high levels of Slug facilitate tumor cell dissemination and metastasis.
Cancer Stem Cells: There is evidence suggesting that EMT, spurred by factors like Slug, can increase the proportion of cancer stem cells (CSCs). These CSCs are thought to be key players in tumor recurrence and maintenance.

General Trend: High Slug expression in various cancers (including breast, colorectal, head and neck, and others) is frequently correlated with a more aggressive phenotype and poorer clinical outcomes.
Var, Various Cancer: Click to Expand ⟱
Cyclooxygenase (COX)-2 overexpression has been noted in various cancers. PI3Ks/AKT pathways are over-activated in several types of cancers.
EGFR altered activity has been noted in various pathological conditions. However, its regulation is an important step in the inhibition of cancer. In this regard, EGCG shows a pivotal role in the inhibition of EGFR activity.
Activating protein-1 transcription factor has been associated with pathogenesis including cancer.
Activation of the sonic hedgehog (Shh) pathway is required for the growth of numerous tissues and organs and recent evidence indicates that this pathway is often recruited to stimulate growth of cancer stem cells (CSCs) and to orchestrate the reprogramming of cancer cells via epithelial mesenchymal transition (EMT). Increased expression of Nanog has been associated with the aggressive nature of certain cancers, highlighting its role in promoting cancer stem cell characteristics.
The aberrant hedgehog (Hh)/GLI signaling pathway causes the formation and progression of a variety of tumors.
The process of cell apoptosis is often accompanied by the destruction of mitochondrial transmembrane potential, which is widely regarded as one of the earliest events in the process of cell apoptosis.
Human malignancies frequently exhibit mutations in the TGF-β pathway, and overactivation of this system is linked to tumor growth by promoting angiogenesis and inhibiting the innate and adaptive antitumor immune responses50.
Several studies have demonstrated that high cyclin D1 expression was observed in cancers including breast, lung, prostate, lymph node and colorectal cancers [23–25].
The oncogene c-myc, which is frequently over-expressed in cancer cells, is involved in the transactivation of most of the glycolytic enzymes including lactate dehydrogenase A (LDHA) and the glucose transporter GLUT1 [51,52]. Thus, c-myc activation is a likely candidate to promote the enhanced glucose uptake and lactate release in the proliferating cancer cell.
Vimentin is overexpressed in various epithelial cancers, including prostate cancer, gastrointestinal tumors, tumors of the central nervous system, breast cancer, malignant melanoma, and lung cancer. Vimentin’s overexpression in cancer correlates well with accelerated tumor growth, invasion, and poor prognosis; however, the role of vimentin in cancer progression remains obscure.
Heat shock proteins (HSPs) are normally induced under environmental stress to serve as chaperones for maintenance of correct protein folding but they are often overexpressed in many cancers, including breast cancer.
Since NQO1 is highly expressed in many solid tumors, including via upregulation of Nrf2, the design of compounds activated by NQO1 and NQO1-targeted drug delivery have been active areas of research.
Since increased Nrf2 gene expression is one of the main mechanisms of cancer cells in resisting chemotherapeutic drugs and survival in oxidative conditions; finding compounds with the ability to suppress Nrf2 gene expression with minimum side effects can be considered an important strategy for increasing the sensitivity of cancer cells to chemotherapy.
Overexpression of c-met stimulates proliferation, migration and invasion in various types of cancer including prostate cancer.
Overexpression of TGFα and EGFR by many carcinomas correlates with the development of cancer metastasis, resistance to chemotherapy and poor prognosis.
More than 50% of human cancers have a mutated nonfunctional p53.


Scientific Papers found: Click to Expand⟱
3383- ART/DHA,    Dihydroartemisinin: A Potential Natural Anticancer Drug
- Review, Var, NA
TumCP↓, Apoptosis↑, TumMeta↓, angioG↓, TumAuto↑, ER Stress↑, ROS↑, Ca+2↑, p38↑, HSP70/HSPA5↓, PPARγ↑, GLUT1↓, Glycolysis↓, PI3K↓, Akt↓, Hif1a↓, PKM2↓, lactateProd↓, GlucoseCon↓, EMT↓, Slug↓, Zeb1↓, ZEB2↓, Twist↓, Snail?, CAFs/TAFs↓, TGF-β↓, p‑STAT3↓, M2 MC↓, uPA↓, HH↓, AXL↓, VEGFR2↓, JNK↑, Beclin-1↑, GRP78/BiP↑, eff↑, eff↑, eff↑, eff↑, eff↑, eff↑, IL4↓, DR5↑, Cyt‑c↑, Fas↑, FADD↑, cl‑PARP↑, cycE/CCNE↓, CDK2↓, CDK4↓, Mcl-1↓, Ki-67↓, Bcl-2↓, CDK6↓, VEGF↓, COX2↓, MMP9↓,
5415- ASA,    The Anti-Metastatic Role of Aspirin in Cancer: A Systematic Review
- Review, Var, NA
TumMeta↓, COX1↓, TXA2↓, AntiAg↑, EMT↓, TumCMig↓, TumCI↓, AMPK↑, cMyc↓, PGE2↓, Dose↑, RadioS↑, PD-L1↓, E-cadherin↑, EMT↓, Slug↓, Vim↓, Twist↓, MMP2↓, MMP9↓, other↑,
3160- Ash,    Withaferin A: A Pleiotropic Anticancer Agent from the Indian Medicinal Plant Withania somnifera (L.) Dunal
- Review, Var, NA
TumCCA↑, H3↑, P21↑, cycA1/CCNA1↓, CycB/CCNB1↓, cycE/CCNE↓, CDC2↓, CHK1↓, Chk2↓, p38↑, MAPK↑, E6↓, E7↓, P53↑, Akt↓, FOXO3↑, ROS↑, γH2AX↑, MMP↓, mitResp↓, eff↑, TumCD↑, Mcl-1↓, ER Stress↑, ATF4↑, ATF3↑, CHOP↑, NOTCH↓, NF-kB↓, Bcl-2↓, STAT3↓, CDK1↓, β-catenin/ZEB1↓, N-cadherin↓, EMT↓, Cyt‑c↑, eff↑, CDK4↓, p‑RB1↓, PARP↑, cl‑Casp3↑, cl‑Casp9↑, NRF2↑, ER-α36↓, LDHA↓, lipid-P↑, AP-1↓, COX2↓, RenoP↑, PDGFR-BB↓, SIRT3↑, MMP2↓, MMP9↓, NADPH↑, NQO1↑, GSR↑, HO-1↑, *SOD2↑, *Prx↑, *Casp3?, eff↑, Snail↓, Slug↓, Vim↓, CSCs↓, HEY1↓, MMPs↓, VEGF↓, uPA↓, *toxicity↓, CDK2↓, CDK4↓, HSP90↓,
2785- CHr,    Emerging cellular and molecular mechanisms underlying anticancer indications of chrysin
- Review, Var, NA
*NF-kB↓, *COX2↓, *iNOS↓, angioG↓, TOP1↓, HDAC↓, TNF-α↓, IL1β↓, cardioP↑, RenoP↑, neuroP↑, LDL↓, BioAv↑, eff↑, cycD1/CCND1↓, hTERT/TERT↓, MMP-10↓, Akt↓, STAT3↓, VEGF↓, EGFR↓, Snail↓, Slug↓, Vim↓, E-cadherin↑, eff↑, TET1↑, ROS↑, mTOR↓, PPARα↓, ER Stress↑, Ca+2↑, ERK↓, MMP↑, Cyt‑c↑, Casp3↑, HK2↓, NRF2↓, HO-1↓, MMP2↓, MMP9↓, Fibronectin↓, GRP78/BiP↑, XBP-1↓, p‑eIF2α↑, *AST↓, ALAT↓, ALP↓, LDH↓, COX2↑, Bcl-xL↓, IL6↓, PGE2↓, iNOS↓, DNAdam↑, UPR↑, Hif1a↓, EMT↓, Twist↓, lipid-P↑, CLDN1↓, PDK1↓, IL10↓, TLR4↓, NOTCH1↑, PARP↑, Mcl-1↓, XIAP↓,
4682- EGCG,    Human cancer stem cells are a target for cancer prevention using (−)-epigallocatechin gallate
- Review, Var, NA
CSCs↓, EMT↓, ChemoSen↑, CD133↓, CD44↓, ALDH1A1↓, Nanog↓, OCT4↓, TumCP↓, Apoptosis↑, p‑GSK‐3β↓, GSK‐3β↑, β-catenin/ZEB1↓, cMyc↓, XIAP↓, Bcl-2↓, survivin↓, Vim↓, Slug↓, Snail↓,
2948- PL,    The promising potential of piperlongumine as an emerging therapeutics for cancer
- Review, Var, NA
tumCV↓, TumCP↓, TumCI↓, angioG↓, EMT↓, TumMeta↓, *hepatoP↑, *lipid-P↓, *GSH↑, cardioP↑, CycB/CCNB1↓, cycD1/CCND1↓, CDK2↓, CDK1↓, CDK4↓, CDK6↓, PCNA↓, Akt↓, mTOR↓, Glycolysis↓, NF-kB↓, IKKα↓, JAK1↓, JAK2↓, STAT3↓, ERK↓, cFos↓, Slug↓, E-cadherin↑, TOP2↓, P53↑, P21↑, Bcl-2↓, BAX↑, Casp3↑, Casp7↑, Casp8↑, p‑HER2/EBBR2↓, HO-1↑, NRF2↑, BIM↑, p‑FOXO3↓, Sp1/3/4↓, cMyc↓, EGFR↓, survivin↓, cMET↓, NQO1↑, SOD2↑, TrxR↓, MDM2↓, p‑eIF2α↑, ATF4↑, CHOP↑, MDA↑, Ki-67↓, MMP9↓, Twist↓, SOX2↓, Nanog↓, OCT4↓, N-cadherin↓, Vim↓, Snail↓, TumW↓, TumCG↓, HK2↓, RB1↓, IL6↓, IL8↓, SOD1↑, RadioS↑, ChemoSen↑, toxicity↓, Sp1/3/4↓, GSH↓, SOD↑,
923- QC,    Quercetin as an innovative therapeutic tool for cancer chemoprevention: Molecular mechanisms and implications in human health
- Review, Var, NA
ROS↑, GSH↓, Ca+2↝, MMP↓, Casp3↑, Casp8↑, Casp9↑, other↓, *ROS↓, *NRF2↑, HO-1↑, TumCCA↑, Inflam↓, STAT3↓, DR5↑, P450↓, MMPs↓, IFN-γ↓, IL6↓, COX2↓, IL8↓, iNOS↓, TNF-α↓, cl‑PARP↑, Apoptosis↑, P53↑, Sp1/3/4↓, survivin↓, TRAILR↑, Casp10↑, DFF45↑, TNFR 1↑, Fas↑, NF-kB↓, IKKα↓, cycD1/CCND1↓, Bcl-2↓, BAX↑, PI3K↓, Akt↓, E-cadherin↓, Vim↓, β-catenin/ZEB1↓, cMyc↓, EMT↓, MMP2↓, NOTCH1↓, MMP7↓, angioG↓, TSP-1↑, CSCs↓, XIAP↓, Snail↓, Slug↓, LEF1↓, P-gp↓, EGFR↓, GSK‐3β↓, mTOR↓, RAGE↓, HSP27↓, VEGF↓, TGF-β↓, COL1↓, COL3A1↓,
3323- SIL,    Anticancer therapeutic potential of silibinin: current trends, scope and relevance
- Review, Var, NA
Inflam↓, angioG↓, antiOx↑, TumMeta↓, TumCP↓, TumCCA↑, TumCD↑, α-SMA↓, p‑Akt↓, p‑STAT3↓, COX2↓, IL6↓, MMP2↓, HIF-1↓, Snail↓, Slug↓, Zeb1↓, NF-kB↓, p‑EGFR↓, JAK2↓, PI3K↓, PD-L1↓, VEGF↓, CDK4↓, CDK2↓, cycD1/CCND1↓, E2Fs↓,

Showing Research Papers: 1 to 8 of 8

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 8

Pathway results for Effect on Cancer / Diseased Cells:


Redox & Oxidative Stress ⓘ

antiOx↑, 1,   ATF3↑, 1,   GSH↓, 2,   GSR↑, 1,   HO-1↓, 1,   HO-1↑, 3,   lipid-P↑, 2,   MDA↑, 1,   NQO1↑, 2,   NRF2↓, 1,   NRF2↑, 2,   ROS↑, 4,   SIRT3↑, 1,   SOD↑, 1,   SOD1↑, 1,   SOD2↑, 1,   TrxR↓, 1,  

Mitochondria & Bioenergetics ⓘ

CDC2↓, 1,   mitResp↓, 1,   MMP↓, 2,   MMP↑, 1,   XIAP↓, 3,  

Core Metabolism/Glycolysis ⓘ

ALAT↓, 1,   AMPK↑, 1,   cMyc↓, 4,   GlucoseCon↓, 1,   Glycolysis↓, 2,   HK2↓, 2,   lactateProd↓, 1,   LDH↓, 1,   LDHA↓, 1,   LDL↓, 1,   NADPH↑, 1,   PDK1↓, 1,   PKM2↓, 1,   PPARα↓, 1,   PPARγ↑, 1,  

Cell Death ⓘ

Akt↓, 5,   p‑Akt↓, 1,   Apoptosis↑, 3,   BAX↑, 2,   Bcl-2↓, 5,   Bcl-xL↓, 1,   BIM↑, 1,   Casp10↑, 1,   Casp3↑, 3,   cl‑Casp3↑, 1,   Casp7↑, 1,   Casp8↑, 2,   Casp9↑, 1,   cl‑Casp9↑, 1,   Chk2↓, 1,   Cyt‑c↑, 3,   DR5↑, 2,   FADD↑, 1,   Fas↑, 2,   HEY1↓, 1,   hTERT/TERT↓, 1,   iNOS↓, 2,   JNK↑, 1,   MAPK↑, 1,   Mcl-1↓, 3,   MDM2↓, 1,   p38↑, 2,   survivin↓, 3,   TNFR 1↑, 1,   TRAILR↑, 1,   TumCD↑, 2,  

Kinase & Signal Transduction ⓘ

p‑HER2/EBBR2↓, 1,   Sp1/3/4↓, 3,  

Transcription & Epigenetics ⓘ

H3↑, 1,   other↓, 1,   other↑, 1,   tumCV↓, 1,  

Protein Folding & ER Stress ⓘ

CHOP↑, 2,   p‑eIF2α↑, 2,   ER Stress↑, 3,   GRP78/BiP↑, 2,   HSP27↓, 1,   HSP70/HSPA5↓, 1,   HSP90↓, 1,   UPR↑, 1,   XBP-1↓, 1,  

Autophagy & Lysosomes ⓘ

Beclin-1↑, 1,   TumAuto↑, 1,  

DNA Damage & Repair ⓘ

CHK1↓, 1,   DFF45↑, 1,   DNAdam↑, 1,   P53↑, 3,   PARP↑, 2,   cl‑PARP↑, 2,   PCNA↓, 1,   γH2AX↑, 1,  

Cell Cycle & Senescence ⓘ

CDK1↓, 2,   CDK2↓, 4,   CDK4↓, 5,   cycA1/CCNA1↓, 1,   CycB/CCNB1↓, 2,   cycD1/CCND1↓, 4,   cycE/CCNE↓, 2,   E2Fs↓, 1,   P21↑, 2,   RB1↓, 1,   p‑RB1↓, 1,   TumCCA↑, 3,  

Proliferation, Differentiation & Cell State ⓘ

ALDH1A1↓, 1,   CD133↓, 1,   CD44↓, 1,   cFos↓, 1,   cMET↓, 1,   CSCs↓, 3,   EMT↓, 8,   ERK↓, 2,   FOXO3↑, 1,   p‑FOXO3↓, 1,   GSK‐3β↓, 1,   GSK‐3β↑, 1,   p‑GSK‐3β↓, 1,   HDAC↓, 1,   HH↓, 1,   mTOR↓, 3,   Nanog↓, 2,   NOTCH↓, 1,   NOTCH1↓, 1,   NOTCH1↑, 1,   OCT4↓, 2,   PI3K↓, 3,   SOX2↓, 1,   STAT3↓, 4,   p‑STAT3↓, 2,   TOP1↓, 1,   TOP2↓, 1,   TumCG↓, 1,  

Migration ⓘ

AntiAg↑, 1,   AP-1↓, 1,   AXL↓, 1,   Ca+2↑, 2,   Ca+2↝, 1,   CAFs/TAFs↓, 1,   CLDN1↓, 1,   COL1↓, 1,   COL3A1↓, 1,   E-cadherin↓, 1,   E-cadherin↑, 3,   ER-α36↓, 1,   Fibronectin↓, 1,   Ki-67↓, 2,   LEF1↓, 1,   MMP-10↓, 1,   MMP2↓, 5,   MMP7↓, 1,   MMP9↓, 5,   MMPs↓, 2,   N-cadherin↓, 2,   RAGE↓, 1,   Slug↓, 8,   Snail?, 1,   Snail↓, 6,   TET1↑, 1,   TGF-β↓, 2,   TSP-1↑, 1,   TumCI↓, 2,   TumCMig↓, 1,   TumCP↓, 4,   TumMeta↓, 4,   Twist↓, 4,   uPA↓, 2,   Vim↓, 6,   Zeb1↓, 2,   ZEB2↓, 1,   α-SMA↓, 1,   β-catenin/ZEB1↓, 3,  

Angiogenesis & Vasculature ⓘ

angioG↓, 5,   ATF4↑, 2,   EGFR↓, 3,   p‑EGFR↓, 1,   HIF-1↓, 1,   Hif1a↓, 2,   PDGFR-BB↓, 1,   TXA2↓, 1,   VEGF↓, 5,   VEGFR2↓, 1,  

Barriers & Transport ⓘ

GLUT1↓, 1,   P-gp↓, 1,  

Immune & Inflammatory Signaling ⓘ

COX1↓, 1,   COX2↓, 4,   COX2↑, 1,   IFN-γ↓, 1,   IKKα↓, 2,   IL10↓, 1,   IL1β↓, 1,   IL4↓, 1,   IL6↓, 4,   IL8↓, 2,   Inflam↓, 2,   JAK1↓, 1,   JAK2↓, 2,   M2 MC↓, 1,   NF-kB↓, 4,   PD-L1↓, 2,   PGE2↓, 2,   TLR4↓, 1,   TNF-α↓, 2,  

Hormonal & Nuclear Receptors ⓘ

CDK6↓, 2,  

Drug Metabolism & Resistance ⓘ

BioAv↑, 1,   ChemoSen↑, 2,   Dose↑, 1,   eff↑, 11,   P450↓, 1,   RadioS↑, 2,  

Clinical Biomarkers ⓘ

ALAT↓, 1,   ALP↓, 1,   E6↓, 1,   E7↓, 1,   EGFR↓, 3,   p‑EGFR↓, 1,   p‑HER2/EBBR2↓, 1,   hTERT/TERT↓, 1,   IL6↓, 4,   Ki-67↓, 2,   LDH↓, 1,   PD-L1↓, 2,   RAGE↓, 1,  

Functional Outcomes ⓘ

cardioP↑, 2,   neuroP↑, 1,   RenoP↑, 2,   toxicity↓, 1,   TumW↓, 1,  
Total Targets: 228

Pathway results for Effect on Normal Cells:


Redox & Oxidative Stress ⓘ

GSH↑, 1,   lipid-P↓, 1,   NRF2↑, 1,   Prx↑, 1,   ROS↓, 1,   SOD2↑, 1,  

Cell Death ⓘ

Casp3?, 1,   iNOS↓, 1,  

Immune & Inflammatory Signaling ⓘ

COX2↓, 1,   NF-kB↓, 1,  

Clinical Biomarkers ⓘ

AST↓, 1,  

Functional Outcomes ⓘ

hepatoP↑, 1,   toxicity↓, 1,  
Total Targets: 13

Scientific Paper Hit Count for: Slug, transcription factor Slug
1 Artemisinin
1 Aspirin -acetylsalicylic acid
1 Ashwagandha(Withaferin A)
1 Chrysin
1 EGCG (Epigallocatechin Gallate)
1 Piperlongumine
1 Quercetin
1 Silymarin (Milk Thistle) silibinin
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:26  Cells:%  prod#:%  Target#:413  State#:%  Dir#:1
  wNotes=0  sortOrder:rid,rpid

 

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