Zeb1 Cancer Research Results

Zeb1, Zinc finger E-box-binding homeobox 1: Click to Expand ⟱
Source:
Type: protein
Transcription factor that promotes tumor invasion and metastasis by inducing epithelial-mesenchymal transition (EMT) in carcinoma cells.
Zinc finger E-box-binding homeobox 1 (ZEB1) is a transcription factor that plays a significant role in various biological processes, including embryonic development, cell differentiation, and epithelial-to-mesenchymal transition (EMT).

By repressing epithelial markers (e.g., E-cadherin) and promoting mesenchymal genes, Zeb1 facilitates cell migration, invasion, and metastasis.

Cancers (such as breast, colorectal, pancreatic, and lung cancers), Zeb1 is frequently upregulated. Zeb1 may be more prominent in specific tumor regions (e.g., invasive fronts) where EMT is actively occurring.
High levels of Zeb1 have been correlated with poor patient outcomes in multiple cancers.


Scientific Papers found: Click to Expand⟱
756- Bor,    Evaluation of Boric Acid Treatment on microRNA‐127‐5p and Metastasis Genes Orchestration of Breast Cancer Stem Cells
- in-vitro, BC, MCF-7
COL1A1↓,
Vim↓,
miR-127-5p↑,
Zeb1↑, expression of the miR-127-5p, ZEB1, CDH1, ITGB1 , ITGA5 , LAMA5 , and SNAIL, was up-regulated in dose-treated BC-SCs
CDH1↑,
ITGB1↑,
ITGA5↑,
LAMA5↑,
Snail↑,

736- Bor,    Evaluation of Boric Acid Treatment on microRNA-127-5p and Metastasis Genes Orchestration of Breast Cancer Stem Cells
- in-vitro, BC, MCF-7
miR-126↑, boric acid could induce miR-127-5p expression
COL1A1↓,
Vim↓,
Zeb1↑, expression of the miR-127-5p, ZEB1, CDH1, ITGB1, ITGA5, LAMA5, and SNAIL, was up-regulated in dose-treated BC-SCs
CDH1↑,
ITGB1↑,
ITGA5↑,
LAMA5↑,
Snail↑,
miR-127-5p↑,

733- Bor,    The analysis of boric acid effect on epithelial-mesenchymal transition of CD133 + CD117 + lung cancer stem cells
- in-vitro, Lung, NA
Snail↑,
ITGB1↑,
ITGA5↑,
COL1A1↓, 50 mM 24 h of BA treatment could be more beneficial as it reduces the expression of COL1A1 in cancer stem cells.
LAMA5↑,
MMP3↓,
Vim↓,
E-cadherin↑,
EMT↓, inhibit the EMT of lung cancer stem cells by reducing E-cadherin and Collagen-1 expression.
Zeb1↑,

3205- EGCG,    The Role of Epigallocatechin-3-Gallate in Autophagy and Endoplasmic Reticulum Stress (ERS)-Induced Apoptosis of Human Diseas
- Review, Var, NA - Review, AD, NA
Beclin-1↑, EGCG not only regulates autophagy via increasing Beclin-1 expression and reactive oxygen species generation,
ROS↑,
Apoptosis↑, Apoptosis is a common cell function in biology and is induced by endoplasmic reticulum stress (ERS)
ER Stress↑,
*Inflam↓, EGCG has health benefits including anti-tumor [15], anti-inflammatory [16], anti-diabetes [17], anti-myocardial infarction [18], anti-cardiac hypertrophy [19], anti-atherosclerosis [20], and antioxidant
*cardioP↑,
*antiOx↑,
*LDL↓, These effects are mainly related to (LDL) cholesterol inhibition, NF-κB inhibition, MPO activity inhibition, decreased levels of glucose and glycated hemoglobin in plasma, decreased inflammatory markers, and reduced ROS generation
*NF-kB↓,
*MPO↓,
*glucose↓,
*ROS↓,
ATG5↑, EGCG induced autophagy by enhancing Beclin-1, ATG5, and LC3B and promoted mitochondrial depolarization in breast cancer cells.
LC3B↑,
MMP↑,
lactateProd↓, 20 mg kg−1 EGCG significantly decreased glucose, lactic acid, and vascular endothelial growth factor (VEGF) levels
VEGF↓,
Zeb1↑, (20 uM) inhibited the proliferation through activating autophagy via upregulating ZEB1, WNT11, IGF1R, FAS, BAK, and BAD genes and inhibiting TP53, MYC, and CASP8 genes in SSC-4 human oral squamous cells [
Wnt↑,
IGF-1R↑,
Fas↑,
Bak↑,
BAD↑,
TP53↓,
Myc↓,
Casp8↓,
LC3II↑, increasing the LC3-II expression levels and induced apoptosis via inducing ROS in mesothelioma cell lines,
NOTCH3↓, but also could reduce partially Notch3/DLL3 to reduce drug-resistance and the stemness of tumor cells
eff↑, In combination therapies, low-intensity pulsed electric field (PEF) can improve EGCG to affect tumor cells; ultrasound (US) with tumor cells is the application of physical stimulation in cancer therapy.
p‑Akt↓, 20 μM EGCG increased intracellular ROS levels and LC3-II, and inhibited p-Akt in PANC-1 cells
PARP↑, 100 μM EGCG increased LC3-II, activated caspase-3 and PARP, and reduced p-Akt in HepG2
*Cyt‑c↓, EGCG protected neuronal cells against human viruses by inhibiting cytochrome c and Bax translocations, and reducing autophagy with increased LC3-II expression and decreased p62 expression
*BAX↓,
*memory↑, EGCG restored autophagy in the mTOR/p70S6K pathway to weaken memory and learning disorders induced by CUMS
*neuroP↑, Finally, EGCG increased the neurological scores through inhibiting cell death
*Ca+2?, EGCG treatment, [Ca2+]m and [Ca2+]i expressions were reduced and oxyhemoglobin-induced mitochondrial dysfunction lessened.
GRP78/BiP↑, MMe cells with EGCG treatment improved GRP78 expression in the endoplasmic reticulum, and induced EDEM, CHOP, XBP1, and ATF4 expressions, and increased the activity of caspase-3 and caspase-8.
CHOP↑, GRP78 accumulation converted UPR of MMe cells into pro-apoptotic ERS
ATF4↑,
Casp3↑,
Casp8↑,
UPR↑,

4699- PTS,    Pterostilbene inhibits triple-negative breast cancer metastasis via inducing microRNA-205 expression and negatively modulates epithelial-to-mesenchymal transition
- in-vitro, BC, MDA-MB-231 - in-vitro, BC, HS587T - in-vivo, BC, MDA-MB-231
TumCMig↓, Pterostilbene inhibited the migratory and invasive potential of triple-negative MDA-MB-231 and Hs578t cells,
TumCI↓,
E-cadherin↑, accompanied by the up-regulation of E-cadherin and down-regulation of Snail, Slug, vimentin and ZEB1.
Snail↓,
Slug↓,
Vim↓,
Zeb1↑,
miR-205↑, significant up-regulation of miR-205, which resulted in the reduction of Src expression in pterostilbene-treated breast cancer cells
Src↓,
TumCG↓, suppressed tumor growth and metastasis in MDA-MB-231-bearing NOD/SCID mice
FAK↓, by reducing Src/Fak signaling
EMT↓, Our findings provide supports for the usage of pterostilbene as an inhibitor of EMT process and potential candidate for adjuvant therapy.


Showing Research Papers: 1 to 5 of 5

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 5

Pathway results for Effect on Cancer / Diseased Cells:


Redox & Oxidative Stress

ROS↑, 1,  

Mitochondria & Bioenergetics

MMP↑, 1,  

Core Metabolism/Glycolysis

lactateProd↓, 1,  

Cell Death

p‑Akt↓, 1,   Apoptosis↑, 1,   BAD↑, 1,   Bak↑, 1,   Casp3↑, 1,   Casp8↓, 1,   Casp8↑, 1,   Fas↑, 1,   miR-127-5p↑, 2,   Myc↓, 1,  

Transcription & Epigenetics

miR-205↑, 1,  

Protein Folding & ER Stress

CHOP↑, 1,   ER Stress↑, 1,   GRP78/BiP↑, 1,   UPR↑, 1,  

Autophagy & Lysosomes

ATG5↑, 1,   Beclin-1↑, 1,   LC3B↑, 1,   LC3II↑, 1,  

DNA Damage & Repair

PARP↑, 1,   TP53↓, 1,  

Proliferation, Differentiation & Cell State

EMT↓, 2,   IGF-1R↑, 1,   NOTCH3↓, 1,   Src↓, 1,   TumCG↓, 1,   Wnt↑, 1,  

Migration

CDH1↑, 2,   COL1A1↓, 3,   E-cadherin↑, 2,   FAK↓, 1,   ITGA5↑, 3,   ITGB1↑, 3,   LAMA5↑, 3,   MMP3↓, 1,   Slug↓, 1,   Snail↓, 1,   Snail↑, 3,   TumCI↓, 1,   TumCMig↓, 1,   Vim↓, 4,   Zeb1↑, 5,  

Angiogenesis & Vasculature

ATF4↑, 1,   miR-126↑, 1,   VEGF↓, 1,  

Drug Metabolism & Resistance

eff↑, 1,  

Clinical Biomarkers

Myc↓, 1,   TP53↓, 1,  
Total Targets: 51

Pathway results for Effect on Normal Cells:


Redox & Oxidative Stress

antiOx↑, 1,   MPO↓, 1,   ROS↓, 1,  

Core Metabolism/Glycolysis

glucose↓, 1,   LDL↓, 1,  

Cell Death

BAX↓, 1,   Cyt‑c↓, 1,  

Migration

Ca+2?, 1,  

Immune & Inflammatory Signaling

Inflam↓, 1,   NF-kB↓, 1,  

Functional Outcomes

cardioP↑, 1,   memory↑, 1,   neuroP↑, 1,  
Total Targets: 13

Scientific Paper Hit Count for: Zeb1, Zinc finger E-box-binding homeobox 1
3 Boron
1 EGCG (Epigallocatechin Gallate)
1 Pterostilbene
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:%  Cells:%  prod#:%  Target#:341  State#:%  Dir#:2
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