EGR1 Cancer Research Results

EGR1, Early Growth Response 1: Click to Expand ⟱
Source:
Type:
Early Growth Response 1 (EGR1). EGR1 is an immediate early response transcription factor that regulates genes linked to cell growth, differentiation, apoptosis, and stress responses.

- EGR1 rapidly induces or suppresses a broad array of target genes involved in cell cycle control, apoptosis, and cell survival.

-Its dualistic nature as both a tumor suppressor and a potential oncogene underscores the importance of context when evaluating its prognostic significance.
Scientific Papers found: Click to Expand⟱
6547- BSB,    Antitumor effects of a-bisabolol against pancreatic cancer
- vitro+vivo, PC, PANC1 - in-vitro, PC, MIA PaCa-2 - in-vitro, PC, KLM1 - in-vitro, PC, KP4 - in-vitro, Nor, ACBRI515
TumCP↓, Bisabolol induced a decrease in cell proliferation and viability in pancreatic cancer cell lines (KLM1, KP4, Panc1, MIA Paca2), but not in pancreatic epithelial cells (ACBRI515).
selectivity↑,
Apoptosis↑, α-Bisabolol treatment induced apoptosis and suppressed Akt activation in pancreatic cancer cell lines.
Akt↓,
EGR1↑, α-bisabolol treatment induced the overexpression of early growth response-1 (EGR1), whereas EGR1 siRNA decreased the α-bisabolol-induced cell death of KLM1 cells.
TumCG↓, Tumor growth in both subcutaneous and peritoneal xenograft nude mouse models was significantly inhibited by intragastric administration of 1000 mg/kg of α-bisabolol, once a week for three weeks.
Dose↝, intragastric administration 1000 mg/kg of α-bisabolol, once a week for three weeks.
PI3K↓, in the present study, we found that a-bisabolol inhibited Akt activation, as well as the expression of its upstream signals (PI3K, PDK1, and mTORC2).
PDK1↓,
mTORC2↑,

2188- SK,    Molecular mechanism of shikonin inhibiting tumor growth and potential application in cancer treatment
- Review, Var, NA
ROS↑, their induction of reactive oxygen species production, inhibition of EGFR and PI3K/AKT signaling pathway activation, inhibition of angiogenesis and induction of apoptosis and necroptosis
EGFR↓,
PI3K↓,
Akt↓,
angioG↓,
Apoptosis↑,
Necroptosis↑,
GSH↓, leading to the increased consumption of reduced glutathione (GSH) and increased Ca2+ concentration in the cells and destroying the mitochondrial membrane potential.
Ca+2↓,
MMP↓,
ERK↓, 24 h of treatment with shikonin, ERK 1/2 and AKT activities were significantly inhibited, and p38 activity was upregulated, which ultimately led to pro-caspase-3 cleavage and triggered the apoptosis of GC cells.
p38↑,
proCasp3↑,
eff↓, pretreated with the ROS scavengers NAC and GSH before treatment with shikonin, the production of ROS was significantly inhibited, the cytotoxicity of shikonin was attenuated
VEGF↓, shikonin can inhibit the expression of VEGF
FOXO3↑, Activated FOXO3a/EGR1/SIRT1 signaling
EGR1↑,
SIRT1↑,
RIP1↑, Upregulation of RIP1 and RIP3
RIP3↑,
BioAv↓, limitations caused by its poor water solubility, it has a short half-life and nonselective biological distribution
NF-kB↓, Shikonin can also prevent the activation of NF-κB by AKT and then downregulate the expression of Bcl-xl,
Half-Life↓, due to the limitations caused by its poor water solubility, it has a short half-life and nonselective biological distribution.


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) ⓘ

GSH↓, 1,   ROS↑, 1,  

Mitochondria & Bioenergetics(tgid=3) ⓘ

MMP↓, 1,  

Core Metabolism/Glycolysis(tgid=4) ⓘ

PDK1↓, 1,   SIRT1↑, 1,  

Cell Death(tgid=5) ⓘ

Akt↓, 2,   Apoptosis↑, 2,   proCasp3↑, 1,   Necroptosis↑, 1,   p38↑, 1,   RIP1↑, 1,  

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

ERK↓, 1,   FOXO3↑, 1,   mTORC2↑, 1,   PI3K↓, 2,   TumCG↓, 1,  

Migration(tgid=13) ⓘ

Ca+2↓, 1,   RIP3↑, 1,   TumCP↓, 1,  

Angiogenesis & Vasculature(tgid=14) ⓘ

angioG↓, 1,   EGFR↓, 1,   EGR1↑, 2,   VEGF↓, 1,  

Immune & Inflammatory Signaling(tgid=16) ⓘ

NF-kB↓, 1,  

Drug Metabolism & Resistance(tgid=21) ⓘ

BioAv↓, 1,   Dose↝, 1,   eff↓, 1,   Half-Life↓, 1,   selectivity↑, 1,  

Clinical Biomarkers(tgid=22) ⓘ

EGFR↓, 1,  
Total Targets: 30

Pathway results for Effect on Normal Cells:


Total Targets: 0

Scientific Paper Hit Count for: EGR1, Early Growth Response 1
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#:1260  State#:%  Dir#:2
  wNotes=on  sortOrder:rid,rpid

 

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