AntiAg Cancer Research Results

AntiAg, Antiplatelet aggregation: Click to Expand ⟱
Source:
Type:
Antiplatelet aggregation refers to the process by which platelets clump together to form a blood clot.
The plethora of evidence indicates that among multiple hemostasis components, platelets play major roles in cancer progression by providing surface and granular contents for several interactions as well as behaving like immune cells.On the other hand, there are suggestions that antiplatelet treatment may promote solid tumor development in a phenomenon described as “cancers follow bleeding.” The controversies around antiplatelet agents justify insight into the subject to establish what, if any, role platelet-directed therapy has in the continuum of anticancer management.
The interplay between antiplatelet aggregation and cancer is an area of active research, with potential implications for therapeutic strategies. Antiplatelet agents, such as aspirin, are being investigated for their role in cancer prevention and treatment, particularly in reducing metastasis and improving patient outcomes.
Scientific Papers found: Click to Expand⟱
6820- EMD,    The Health Benefits of Emodin, a Natural Anthraquinone Derived from Rhubarb—A Summary Update
- Review, Nor, NA - Review, Arthritis, NA - Review, AD, NA
*diuretic↑, Emodin has a wide range of biological activities, including diuretic, antibacterial, antiulcer, anti-inflammatory, anticancer and antinociceptive.
*Bacteria↓,
*Inflam↓,
AntiCan↑,
TumCP↓, emodin inhibits processes of neoplasia at the stages of proliferation, invasion and angiogenesis.
TumCI↓,
angioG↓,
*toxicity↓, The results showed that administration of emodin at the doses of 20, 40, and 80 mg/kg for 12 weeks is safe and did not cause any pathophysiological disorders in major organs in mammals.
IFN-γ↑, more interferon gamma (IFN-γ), interleukin (IL)-12 and reactive oxygen species (ROS) and less IL-6, tumor necrosis factor alpha (TNF-α) and transforming growth factor beta1 (TGF-β1) in he alveolar cavity in the emodin group than those in the control
IL12↑,
ROS↑, In vitro, emodin at the dose of 20 μM had no effect on cell viability in HL-60N1, but increased ROS and decreased autophagy, and thus induced apoptosis in HL-60N2
TNF-α↓,
TNF-α↓,
TGF-β↓,
MAPK↓, Antitumor properties of emodin are associated with inhibiting the activity of tyrosine kinases, such as mitogen-activated protein kinase (MAPK), protein kinase C (PKC), factor kappa-light-chain-enhancer of activated B cells (NF-κB)
PKCδ↓,
NF-kB↓,
HER2/EBBR2↓, emodin suppresses the activity of HER-2/neu tyrosine kinase [55]; whereas, in colon cancer cells, emodin inhibits phosphorylation of vascular endothelial growth factor (VEGF)
VEGF↓,
DNAdam↑, Another antiproliferative mechanism of emodin activity involves induction of DNA damage by the ROS, whose concentration is considerably increased in the cells treated with this anthraquinone.
Necroptosis↑, emodin induces necroptosis in the cells of renal cancer (RCC), which is resistant to conventional cancer therapy, such as chemotherapy or radiotherapy.
Glycolysis↓, and also inhibits glycolysis by downregulation of GLUT1 through ROS-mediated inactivation of the phosphoinositide 3-kinases (PI3K)/AKT signaling pathway.
GLUT1↓,
PI3K↓,
Akt↓,
Casp9↑, increasing active caspase-9, active caspase-3, and bcl-2-like protein 4 (Bax) levels and downregulating Bcl-2.
Casp3↑,
BAX↑,
Bcl-2↓,
eff↑, Li et al. [61] revealed that a bifunctional molecule of β-dihydro-artemisinin-emodin has high antiproliferative activity (suppressing Ki-67 expression),
MMP2↓, Emodin effectively inhibits the expression of the angiogenic-related NF-kB factor, as well as its regulatory factors, including VEGF, MMP-2, MMP-9.
MMP9↓,
eff↑, Combinatorial therapy with emodin and thymoquinone was also efficient in attenuating migration of MCF-7 breast cancer cells, inducing apoptosis, inhibiting cell proliferation, while enhancing cytotoxicity
ChemoSen↑, For example, combination therapy using emodin and doxorubicin sensitize breast cancer cells to doxorubicin by inhibition of proliferation in the DNA damage pathway
P-gp↓, It was demonstrated that emodin downregulated Pgp expression, and enhanced cisplatin-induced apoptosis and DNA damage in the cancer cells
SREBP2↓, suppressing the cholesterol biosynthesis (inhibition the activity of SREBP-2 protein) and inhibiting the expression of the AKT.
eff↑, emodin combined with berberine significantly inhibited the activity of salt-inducible kinases 3 (SIK3), belonging to the AMPK-related kinases, which elevated expressions in breast cancer cells contributing to tumorigenesis.
*other↝, emodin has therapeutic potential for the treatment of various kinds of inflammation, such as pancreatitis, asthma, arthritis, atherosclerosis, myocarditis, glomerulonephritis and Alzheimer’s disease.
*COX2↓, Therapeutic properties of emodin in the treatment of joint inflammation are also associated with inhibition of expression of VEGF, cyclooxygenase 2 (COX-2), hypoxia-inducible factor 1 (HIF-1)α and histone deacetylase (HDAC).
*Hif1a↓,
*HDAC↓,
*tau↓, Emodin effectively prevents abnormal aggregation of tau proteins in PHFs
*PKCδ↑, emodin improved cognitive functions by activating the protein kinase C signaling pathway (PKC), attenuating oxidative stress and inflammatory response in mice with Alzheimer’s disease.
*ROS↓,
*Inflam↓,
AntiAg?,


Showing Research Papers: 1 to 1 of 1

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 1

Pathway results for Effect on Cancer / Diseased Cells:


Redox & Oxidative Stress(tgid=1) ⓘ

ROS↑, 1,  

Core Metabolism/Glycolysis(tgid=4) ⓘ

Glycolysis↓, 1,   SREBP2↓, 1,  

Cell Death(tgid=5) ⓘ

Akt↓, 1,   BAX↑, 1,   Bcl-2↓, 1,   Casp3↑, 1,   Casp9↑, 1,   MAPK↓, 1,   Necroptosis↑, 1,  

Kinase & Signal Transduction(tgid=6) ⓘ

HER2/EBBR2↓, 1,  

DNA Damage & Repair(tgid=10) ⓘ

DNAdam↑, 1,  

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

PI3K↓, 1,  

Migration(tgid=13) ⓘ

AntiAg?, 1,   MMP2↓, 1,   MMP9↓, 1,   PKCδ↓, 1,   TGF-β↓, 1,   TumCI↓, 1,   TumCP↓, 1,  

Angiogenesis & Vasculature(tgid=14) ⓘ

angioG↓, 1,   VEGF↓, 1,  

Barriers & Transport(tgid=15) ⓘ

GLUT1↓, 1,   P-gp↓, 1,  

Immune & Inflammatory Signaling(tgid=16) ⓘ

IFN-γ↑, 1,   IL12↑, 1,   NF-kB↓, 1,   TNF-α↓, 2,  

Drug Metabolism & Resistance(tgid=21) ⓘ

ChemoSen↑, 1,   eff↑, 3,  

Clinical Biomarkers(tgid=22) ⓘ

HER2/EBBR2↓, 1,  

Functional Outcomes(tgid=23) ⓘ

AntiCan↑, 1,  
Total Targets: 32

Pathway results for Effect on Normal Cells:


NA, unassigned(tgid=0) ⓘ

diuretic↑, 1,  

Redox & Oxidative Stress(tgid=1) ⓘ

ROS↓, 1,  

Transcription & Epigenetics(tgid=7) ⓘ

other↝, 1,  

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

HDAC↓, 1,  

Migration(tgid=13) ⓘ

PKCδ↑, 1,  

Angiogenesis & Vasculature(tgid=14) ⓘ

Hif1a↓, 1,  

Immune & Inflammatory Signaling(tgid=16) ⓘ

COX2↓, 1,   Inflam↓, 2,  

Synaptic & Neurotransmission(tgid=18) ⓘ

tau↓, 1,  

Functional Outcomes(tgid=23) ⓘ

toxicity↓, 1,  

Infection & Microbiome(tgid=24) ⓘ

Bacteria↓, 1,  
Total Targets: 11

Scientific Paper Hit Count for: AntiAg, Antiplatelet aggregation
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#:10  State#:%  Dir#:0
  wNotes=on  sortOrder:rid,rpid

 

Home Page