E2Fs Cancer Research Results

E2Fs, E2F family of transcription factors: Click to Expand ⟱
Source: HalifaxProj(inactivate)
Type:
E2Fs have been classified as transcriptional activators (E2F1-3) or transcriptional repressors (E2F4-8), and are thus predicted to play a dual role in human cancers.
Activators: E2F1,2,3a,3b
Repressors: E2F4,5,6,7a,7b,8
As a tumor suppressor and oncogene, the transcription factor E2F1 is a downstream regulator of the Rb pathway.
The role of E2Fs in CSCs is widely regarded as an activator gene. Up-regulation of E2Fs is reported to be involved in proliferation promotion (21), maintenance and acquisition of self-renewal (22, 23), invasion and metastatic progression (24) and resistance to chemotherapy and radiotherapy (25) in many CSCs.
Scientific Papers found: Click to Expand⟱
3201- EGCG,    Epigallocatechin Gallate (EGCG): Pharmacological Properties, Biological Activities and Therapeutic Potential
- Review, NA, NA
*AntiCan↑, EGCG’s therapeutic potential in preventing and managing a range of chronic conditions, including cancer, cardiovascular diseases, neurodegenerative disorders, and metabolic syndromes
*cardioP↑,
*neuroP↑,
*BioAv↝, Factors such as fasting, storage conditions, albumin levels, vitamin C, fish oil, and piperine have been shown to affect plasma concentrations and the overall bioavailability of EGCG
*BioAv↓, Conversely, bioavailability is reduced by processes such as air oxidation, sulfation, glucuronidation, gastrointestinal degradation, and interactions with Ca2+, Mg2+, and trace metals,
*BioAv↓, EGCG’s oral bioavailability is generally low, with marked differences observed across species, for example, bioavailability rates of 26.5% in CF-1 mice and just 1.6% in Sprague Dawley rats
*Dose↝, plasma concentrations exceeded 1 μM only when doses of 1 g or higher were administered.
*Half-Life↝, Specifically, a dose of 1600 mg yielded a Cmax of 3392 ng/mL (range: 130–3392 ng/mL), with peak levels observed between 1.3 and 2.2 h, AUC (0–∞) values ranging from 442 to 10,368 ng·h/mL, and a half-life (t1/2z) of 1.9 to 4.6 h.
*BioAv↑, Studies on the distribution of EGCG have revealed that, despite its limited absorption, it is rapidly disseminated throughout the body or quickly converted into metabolites
*BBB↑, Additionally, EGCG can cross the blood–brain barrier, allowing it to reach the brain
*hepatoP↓, Several studies have documented liver damage linked to green tea consumption [48,49,50,51,52,53].
*other↓, EGCG has also been shown to inhibit the intestinal absorption of non-heme iron in a dose-dependent manner in a controlled clinical trial
*Inflam↓, EGCG has been widely recognized for its anti-inflammatory effects
*NF-kB↓, EGCG has been shown to suppress NF-κB activation, inhibit its nuclear translocation, and block AP-1 activity
*AP-1↓,
*iNOS↓, downregulation of pro-inflammatory enzymes like iNOS and COX-2 and scavenging of ROS/RNS, including nitric oxide and peroxynitrite
*COX2↓,
*ROS↓,
*RNS↓,
*IL8↓, EGCG has been shown to suppress airway inflammation by reducing IL-8 release, a cytokine involved in neutrophil aggregation and ROS production.
*JAK↓, EGCG blocks the JAK1/2 signaling pathway
*PDGFR-BB↓, downregulate PDGFR and IGF-1R gene expression
*IGF-1R↓,
*MMP2↓, reduce MMP-2 mRNA expression
*P53↓, downregulation of the p53-p21 signaling pathway and the enhanced expression of Nrf2
*NRF2↑,
*TNF-α↓, 25 to 100 μM reduced the levels of TNF-α, IL-6, and ROS while enhancing the expression of E2F2 and superoxide dismutases (SOD1 and SOD2), enzymes vital for cellular antioxidant defense.
*IL6↓,
*E2Fs↑,
*SOD1↑,
*SOD2↑,
Casp3↑, EGCG has been shown to activate key apoptotic pathways, such as caspase-3 activation, cytochrome c release, and PARP cleavage, in various cell models, including PC12 cells exposed to oxidative stress
Cyt‑c↑,
PARP↑,
DNMTs↓, (1) the inhibition of DNA hypermethylation by blocking DNA methyltransferase (DNMT)
Telomerase↓, (2) the repression of telomerase activity;
Hif1a↓, (3) the suppression of angiogenesis via the inhibition of HIF-1α and NF-κB;
MMPs↓, (4) the prevention of cellular metastasis by inhibiting matrix metalloproteinases (MMPs);
BAX↑, (5) the promotion of apoptosis through the activation of pro-apoptotic proteins like BAX and BAK
Bak↑,
Bcl-2↓, while downregulating anti-apoptotic proteins like BCL-2 and BCL-XL;
Bcl-xL↓,
P53↑, (6) the upregulation of tumor suppressor genes such as p53 and PTEN;
PTEN↑,
TumCP↓, (7) the inhibition of inflammation and proliferation via NF-κB suppression;
MAPK↓, (8) anti-proliferative activity through the modulation of MAPK and IGF1R pathways
HGF/c-Met↓, EGCG inhibits hepatocyte growth factor (HGF), which is involved in tumor migration and invasion
TIMP1↑, EGCG has also been shown to influence the expression of tissue inhibitors of metalloproteinases (TIMPs) and MMPs, which are involved in tumorigenesis
HDAC↓, nhibition of UVB-induced DNA hypomethylation and modulation of DNMT and histone deacetylase (HDAC) activities
MMP9↓, inhibiting MMPs such as MMP-2 and MMP-9
uPA↓, EGCG may block urokinase-like plasminogen activator (uPA), a protease involved in cancer progression
GlutMet↓, EGCG can exert antitumor effects by inhibiting glycolytic enzymes, reducing glucose metabolism, and further suppressing cancer-cell growth
ChemoSen↑, EGCG’s combination with standard chemotherapy drugs may enhance their efficacy through additive or synergistic effects, while also mitigating chemotherapy-related side effects
chemoP↑,

3479- MF,    Evaluation of Pulsed Electromagnetic Field Effects: A Systematic Review and Meta-Analysis on Highlights of Two Decades of Research In Vitro Studies
- Review, NA, NA
*eff↓, evidence suggests that frequencies higher than 100 Hz, flux densities between 1 and 10 mT, and chronic exposure more than 10 days would be more effective in establishing a cellular response
eff↝, undifferentiated PC12 cells are more sensitive to PEMF exposure, while differentiated PC12 cells are more resistant to stress
*Hif1a↑, Retinal pigment epithelial (RPE) cells Frequency of 50 Hz Intensity of 1 mT : HIF-1α, VEGFA, VEGFR-2, CTGF, cathepsin D TIMP-1, E2F3, MMP-2, and MMP-9) increased
*VEGF↑,
*TIMP1↑,
*E2Fs↑,
*MMP2↑,
*MMP9↑,
Apoptosis↑, MCF7, MCF10 Frequencies of 20 and 50 Hz Intensities of 2.0, 3.0, and 5.0 mT Cell apoptosis

5022- UA,    Ursolic Acid’s Alluring Journey: One Triterpenoid vs. Cancer Hallmarks
- Review, Var, NA
TumCP↓, inhibition of cell proliferation, induction of apoptosis, suppression of angiogenesis, inhibition of metastasis, and modulation of the tumor microenvironment
Apoptosis↑,
angioG↑,
TumMeta↓,
BioAv↓, acknowledges hurdles related to UA’s low bioavailability,
Hif1a↓, graphical abstract
Glycolysis↓,
mitResp↓,
Akt↓,
MAPK↓,
ERK↓,
mTOR↓,
P53↑,
P21↑,
E2Fs↑,
STAT3↓,
MMP↓,
NLRP3↓,
iNOS↓,
CHK1↓,
Chk2↓,
BRCA1↓,
E-cadherin↑,
N-cadherin↓,
Casp↑,
p62↓,
LC3II↑,
Vim↓,
ROS↑, administration of UA has effectively modulated the generation of both cellular and mitochondrial ROS
CSCs↓, This, in turn, triggers a response in embryonic CSCs known as DNA damage response (DDR), strongly suggesting the potential for UA-induced cell death
DNAdam↑,
GutMicro↑, UA has shown potential in modulating the composition of the gut microbiota and improving the microenvironment within the digestive system
VEGF↓, UA treatment significantly reduced the expression of VEGF-A and FGF-β in both CRC tumors and HT-29 cells (


Showing Research Papers: 1 to 3 of 3

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 3

Pathway results for Effect on Cancer / Diseased Cells:


Redox & Oxidative Stress ⓘ

ROS↑, 1,  

Mitochondria & Bioenergetics ⓘ

mitResp↓, 1,   MMP↓, 1,  

Core Metabolism/Glycolysis ⓘ

GlutMet↓, 1,   Glycolysis↓, 1,  

Cell Death ⓘ

Akt↓, 1,   Apoptosis↑, 2,   Bak↑, 1,   BAX↑, 1,   Bcl-2↓, 1,   Bcl-xL↓, 1,   Casp↑, 1,   Casp3↑, 1,   Chk2↓, 1,   Cyt‑c↑, 1,   HGF/c-Met↓, 1,   iNOS↓, 1,   MAPK↓, 2,   Telomerase↓, 1,  

Autophagy & Lysosomes ⓘ

LC3II↑, 1,   p62↓, 1,  

DNA Damage & Repair ⓘ

BRCA1↓, 1,   CHK1↓, 1,   DNAdam↑, 1,   DNMTs↓, 1,   P53↑, 2,   PARP↑, 1,  

Cell Cycle & Senescence ⓘ

E2Fs↑, 1,   P21↑, 1,  

Proliferation, Differentiation & Cell State ⓘ

CSCs↓, 1,   ERK↓, 1,   HDAC↓, 1,   mTOR↓, 1,   PTEN↑, 1,   STAT3↓, 1,  

Migration ⓘ

E-cadherin↑, 1,   MMP9↓, 1,   MMPs↓, 1,   N-cadherin↓, 1,   TIMP1↑, 1,   TumCP↓, 2,   TumMeta↓, 1,   uPA↓, 1,   Vim↓, 1,  

Angiogenesis & Vasculature ⓘ

angioG↑, 1,   Hif1a↓, 2,   VEGF↓, 1,  

Protein Aggregation ⓘ

NLRP3↓, 1,  

Drug Metabolism & Resistance ⓘ

BioAv↓, 1,   ChemoSen↑, 1,   eff↝, 1,  

Clinical Biomarkers ⓘ

BRCA1↓, 1,   GutMicro↑, 1,  

Functional Outcomes ⓘ

chemoP↑, 1,  
Total Targets: 54

Pathway results for Effect on Normal Cells:


Redox & Oxidative Stress ⓘ

NRF2↑, 1,   RNS↓, 1,   ROS↓, 1,   SOD1↑, 1,   SOD2↑, 1,  

Cell Death ⓘ

iNOS↓, 1,  

Transcription & Epigenetics ⓘ

other↓, 1,  

DNA Damage & Repair ⓘ

P53↓, 1,  

Cell Cycle & Senescence ⓘ

E2Fs↑, 2,  

Proliferation, Differentiation & Cell State ⓘ

IGF-1R↓, 1,  

Migration ⓘ

AP-1↓, 1,   MMP2↓, 1,   MMP2↑, 1,   MMP9↑, 1,   TIMP1↑, 1,  

Angiogenesis & Vasculature ⓘ

Hif1a↑, 1,   PDGFR-BB↓, 1,   VEGF↑, 1,  

Barriers & Transport ⓘ

BBB↑, 1,  

Immune & Inflammatory Signaling ⓘ

COX2↓, 1,   IL6↓, 1,   IL8↓, 1,   Inflam↓, 1,   JAK↓, 1,   NF-kB↓, 1,   TNF-α↓, 1,  

Drug Metabolism & Resistance ⓘ

BioAv↓, 2,   BioAv↑, 1,   BioAv↝, 1,   Dose↝, 1,   eff↓, 1,   Half-Life↝, 1,  

Clinical Biomarkers ⓘ

IL6↓, 1,  

Functional Outcomes ⓘ

AntiCan↑, 1,   cardioP↑, 1,   hepatoP↓, 1,   neuroP↑, 1,  
Total Targets: 37

Scientific Paper Hit Count for: E2Fs, E2F family of transcription factors
1 EGCG (Epigallocatechin Gallate)
1 Magnetic Fields
1 Ursolic 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

Filter Conditions: Pro/AntiFlg:%  IllCat:%  CanType:%  Cells:%  prod#:%  Target#:90  State#:%  Dir#:2
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