eNOS Cancer Research Results

eNOS, endothelial Nitric Oxide Synthase: Click to Expand ⟱
Source:
Type:
Endothelial Nitric Oxide Synthase is an enzyme that is constitutively expressed in endothelial cells, which line the blood vessels.
-Vascular Signaling, Angiogenesis, and Context-Dependent Effects
-It generates nitric oxide (NO) from L-arginine in a calcium/calmodulin- and phosphorylation-dependent manner.

eNOS is a vascular and microenvironmental regulator that usually supports cancer by enabling angiogenesis, perfusion, and survival signaling. Its effects are highly context-dependent—beneficial for normal tissue homeostasis, but often co-opted by tumors to sustain growth and resist therapy. Therapeutic strategies typically modulate upstream pathways rather than directly targeting eNOS itself.
Scientific Papers found: Click to Expand⟱
3455- ALA,    Alpha-lipoic acid inhibits proliferation and migration of human vascular endothelial cells through downregulating HSPA12B/VEGF signaling axis
- in-vitro, Nor, HUVECs
*cMyc↓, The expressions of C-Myc, VEGF, and eNOS and phosphorylation of focal adhesion kinase were reduced by LA.
*VEGF↓,
*eNOS↓,
angioG↓, LA might represent a viable therapeutic potential for human diseases that involve high angiogenic activities such as cancers.

1150- Api,    Apigenin inhibits the TNFα-induced expression of eNOS and MMP-9 via modulating Akt signalling through oestrogen receptor engagement
- in-vitro, Lung, EAhy926
eNOS↓, Apigenin (50 μM) counteracted the TNFα-induced expression of eNOS and MMP-9 and the TNFα- triggered activation of Akt, p38MAPK and JNK signalling
MMP9↓,
Akt↓,
p38↓,
JNK↓, Apigenin pre-treatment (50 lM) significantly inhibited the TNFa-induced phosphorylation of Akt (Fig. 2a), p38MAPK (Fig. 2b) and JNK

1322- EMD,    The versatile emodin: A natural easily acquired anthraquinone possesses promising anticancer properties against a variety of cancers
- Review, Var, NA
Apoptosis↑,
TumCP↓,
ROS↑,
TumAuto↑,
EMT↓,
TGF-β↓,
DNAdam↑,
ER Stress↑,
TumCCA↑,
ATP↓,
NF-kB↓,
CYP1A1↑,
STAC2↓,
JAK↓,
PI3K↓,
Akt↓,
MAPK↓,
FASN↓,
HER2/EBBR2↓,
ChemoSen↑, DOX combined with emodin can improve the sensitivity of MDA-MB-231 and MCF-7 cells to chemotherapy
eff↑, emodin was reported to increase the anti-proliferative effect of an EGFR inhibitor (afatinib) against PC through downregulation of EGFR by promoting STAT3
ChemoSen↑, gemcitabine combined with emodin increased cell death
angioG↓,
VEGF↓,
MMP2↓,
eNOS↓,
FOXD3↑,
MMP9↓,
TIMP1↑,

2845- FIS,    Fisetin: A bioactive phytochemical with potential for cancer prevention and pharmacotherapy
- Review, Var, NA
PI3K↓, block multiple signaling pathways such as the phosphatidylinositol-3-kinase/protein kinase B/mammalian target of rapamycin (PI3K/Akt/mTOR) and p38
Akt↓,
mTOR↓,
p38↓,
*antiOx↑, antioxidant, anti-inflammatory, antiangiogenic, hypolipidemic, neuroprotective, and antitumor effect
*neuroP↑,
Casp3↑, U266 cancer cell line through activation of caspase-3, downregulation of Bcl-2 and Mcl-1L, upregulation of Bax, Bim and Bad
Bcl-2↓,
Mcl-1↓,
BAX↑,
BIM↑,
BAD↑,
AMPK↑, activation of 5'adenosine monophosphate-activated protein kinase (AMPK), acetyl-CoA carboxylase (ACC) and decreased phosphorylation of AKT and mTOR were also observed
ACC↑,
DNAdam↑, DNA fragmentation, mitochondrial membrane depolarizatio
MMP↓,
eff↑, fisetin in combination with a citrus flavanone, hesperetin mediated apoptosis by mitochondrial membrane depolarization and caspase-3 act
ROS↑, NCI-H460 human non-small cell lung cancer line, fisetin generated reactive oxygen species (ROS), endoplasmic reticulum (ER) stress
cl‑PARP↑, fisetin treatment resulted in PARP cleavage
Cyt‑c↑, release of cyt. c
Diablo↑, release of cyt. c and Smac/DIABLO from mitochondria,
P53↑, increased p53 protein levels
p65↓, reduced phospho-p65 and Myc oncogene expression
Myc↓,
HSP70/HSPA5↓, fisetin causes inhibition of proliferation by the modulation of heat shock protein 70 (HSP70), HSP27
HSP27↓,
COX2↓, anti-proliferative effects of fisetin through the activation of apoptosis via inhibition of cyclooxygenase-2 (COX-2) and Wnt/EGFR/NF-κB signaling pathways
Wnt↓,
EGFR↓,
NF-kB↓,
TumCCA↑, The anti-proliferative effects of fisetin and hesperetin were shown to be occurred through S, G2/M, and G0/G1 phase arrest in K562 cell progression
CDK2↓, decrease in levels of cyclin D1, cyclin A, Cdk-4 and Cdk-2
CDK4↓,
cycD1/CCND1↓,
cycA1/CCNA1↓,
P21↑, increase in p21 CIP1/WAF1 levels in HT-29 human colon cancer cell
MMP2↓, fisetin has exhibited tumor inhibitory effects by blocking matrix metalloproteinase-2 (MMP- 2) and MMP-9 at mRNA and protein levels,
MMP9↓,
TumMeta↓, Antimetastasis
MMP1↓, fisetin also inhibited the MMP-14, MMP-1, MMP-3, MMP-7, and MMP-9
MMP3↓,
MMP7↓,
MET↓, promotion of mesenchymal to epithelial transition associated with a decrease in mesenchymal markers i.e. N-cadherin, vimentin, snail and fibronectin and an increase in epithelial markers i.e. E-cadherin
N-cadherin↓,
Vim↓,
Snail↓,
Fibronectin↓,
E-cadherin↑,
uPA↓, fisetin suppressed the expression and activity of urokinase plasminogen activator (uPA)
ChemoSen↑, combination treatment of fisetin and sorafenib reduced the migration and invasion of BRAF-mutated melanoma cells both in in-vitro
EMT↓, inhibited epithelial to mesenchymal transition (EMT) as observed by a decrease in N-cadherin, vimentin and fibronectin and an increase in E-cadherin
Twist↓, inhibited expression of Snail1, Twist1, Slug, ZEB1 and MMP-2 and MMP-9
Zeb1↓,
cFos↓, significant decrease in NF-κB, c-Fos, and c-Jun levels
cJun↓,
EGF↓, Fisetin inhibited epidermal growth factor (EGF)
angioG↓, Antiangiogenesis
VEGF↓, decreased expression of endothelial nitric oxide synthase (eNOS) and VEGF, EGFR, COX-2
eNOS↓,
*NRF2↑, significantly increased nuclear translocation of Nrf2 and antioxidant response element (ARE) luciferase activity, leading to upregulation of HO-1 expression
HO-1↑,
NRF2↓, Fisetin also triggered the suppression of Nrf2
GSTs↓, declined placental type glutathione S-transferase (GST-p) level in the liver of the fisetin- treated rats with hepatocellular carcinoma (HCC)
ATF4↓, Fisetin also rapidly increased the levels of both Nrf2 and ATF4

3007- RosA,    Hepatoprotective effects of rosmarinic acid: Insight into its mechanisms of action
- Review, NA, NA
*ROS↓, antioxidant properties as a ROS scavenger and lipid peroxidation inhibitor, anti-inflammatory, neuroprotective and antiangiogenic among others.
*lipid-P↓,
*Inflam↓,
*neuroP↑,
*angioG↓,
*eff↑, The hepatoprotective effects of RA alone and in combination with caffeic acid (CA) was reported in t-BHP-induced oxidative liver damage
*AST↓, significant reduction of indicators of hepatic toxicity, such as AST, ALT, GSSG, lipid peroxidation.
*ALAT↓,
*GSSG↓,
*eNOS↓, It also reduced the liver content of eNOS/iNOS and NO, attenuated NF-κB activation
*iNOS↓,
*NO↓,
*NF-kB↓,
*MMP2↓, It inhibited MMP-2 activity and suppressed ROS generation and lipid peroxidation.
*MDA↓, It also decreased malondialdehyde (MDA) and TNF-α levels while increasing GSH levels as well as SOD and GSH-Px activities in the livers and kidneys.
*TNF-α↓,
*GSH↑,
*SOD↑,
*IL6↓, RA decreased the hepatic level of IL-6, TNF-Alpha, and PGE2, as well as the activity of COX-2 It also decreased hepatic RAGE and sorbitol levels, and GLO-1 activity
*PGE2↓,
*COX2↓,
*mTOR↑, In the study, it was observed that RA stimulated hepatocyte proliferation. Specifically activated the mTOR signaling pathway during liver regeneration and rescued PH-impaired liver functions

1434- SFN,  GEM,    Sulforaphane Potentiates Gemcitabine-Mediated Anti-Cancer Effects against Intrahepatic Cholangiocarcinoma by Inhibiting HDAC Activity
- in-vitro, CCA, HuCCT1 - in-vitro, CCA, HuH28 - in-vivo, NA, NA
HDAC↓,
ac‑H3↑,
ChemoSen↑, SFN synergistically augmented the GEM-mediated attenuation of cell viability and proliferation
tumCV↓,
TumCP↓,
TumCCA↑, G2/M cell cycle arrest
Apoptosis↑,
cl‑Casp3↑,
TumCI↓,
VEGF↓, VEGFA
VEGFR2↓,
Hif1a↓,
eNOS↓,
EMT?, SFN effectively inhibited the GEM-mediated induction of epithelial–mesenchymal transition (EMT)
TumCG↓,
Ki-67↓,
TUNEL↑, increased TUNEL+ apoptotic cells
P21↑,
p‑Chk2↑,
CDC25↓, decreased p-Cdc25C
BAX↑,
*ROS↓, SFN is also known to exert anti-oxidative effects via Nrf2 activation. in vivo study, optimization is performed by evaluating the anti-oxidative property of SFN in the liver.
NQO1?, identified 50 mg/kg/day as the minimal dose that significantly induced these anti-oxidative genes


Showing Research Papers: 1 to 6 of 6

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 6

Pathway results for Effect on Cancer / Diseased Cells:


Redox & Oxidative Stress ⓘ

CYP1A1↑, 1,   GSTs↓, 1,   HO-1↑, 1,   NQO1?, 1,   NRF2↓, 1,   ROS↑, 2,  

Mitochondria & Bioenergetics ⓘ

ATP↓, 1,   CDC25↓, 1,   EGF↓, 1,   MMP↓, 1,  

Core Metabolism/Glycolysis ⓘ

ACC↑, 1,   AMPK↑, 1,   FASN↓, 1,  

Cell Death ⓘ

Akt↓, 3,   Apoptosis↑, 2,   BAD↑, 1,   BAX↑, 2,   Bcl-2↓, 1,   BIM↑, 1,   Casp3↑, 1,   cl‑Casp3↑, 1,   p‑Chk2↑, 1,   Cyt‑c↑, 1,   Diablo↑, 1,   JNK↓, 1,   MAPK↓, 1,   Mcl-1↓, 1,   Myc↓, 1,   p38↓, 2,   TUNEL↑, 1,  

Kinase & Signal Transduction ⓘ

FOXD3↑, 1,   HER2/EBBR2↓, 1,  

Transcription & Epigenetics ⓘ

cJun↓, 1,   ac‑H3↑, 1,   tumCV↓, 1,  

Protein Folding & ER Stress ⓘ

ER Stress↑, 1,   HSP27↓, 1,   HSP70/HSPA5↓, 1,  

Autophagy & Lysosomes ⓘ

TumAuto↑, 1,  

DNA Damage & Repair ⓘ

DNAdam↑, 2,   P53↑, 1,   cl‑PARP↑, 1,  

Cell Cycle & Senescence ⓘ

CDK2↓, 1,   CDK4↓, 1,   cycA1/CCNA1↓, 1,   cycD1/CCND1↓, 1,   P21↑, 2,   TumCCA↑, 3,  

Proliferation, Differentiation & Cell State ⓘ

cFos↓, 1,   EMT?, 1,   EMT↓, 2,   HDAC↓, 1,   mTOR↓, 1,   PI3K↓, 2,   TumCG↓, 1,   Wnt↓, 1,  

Migration ⓘ

E-cadherin↑, 1,   Fibronectin↓, 1,   Ki-67↓, 1,   MET↓, 1,   MMP1↓, 1,   MMP2↓, 2,   MMP3↓, 1,   MMP7↓, 1,   MMP9↓, 3,   N-cadherin↓, 1,   Snail↓, 1,   STAC2↓, 1,   TGF-β↓, 1,   TIMP1↑, 1,   TumCI↓, 1,   TumCP↓, 2,   TumMeta↓, 1,   Twist↓, 1,   uPA↓, 1,   Vim↓, 1,   Zeb1↓, 1,  

Angiogenesis & Vasculature ⓘ

angioG↓, 3,   ATF4↓, 1,   EGFR↓, 1,   eNOS↓, 4,   Hif1a↓, 1,   VEGF↓, 3,   VEGFR2↓, 1,  

Immune & Inflammatory Signaling ⓘ

COX2↓, 1,   JAK↓, 1,   NF-kB↓, 2,   p65↓, 1,  

Drug Metabolism & Resistance ⓘ

ChemoSen↑, 4,   eff↑, 2,  

Clinical Biomarkers ⓘ

EGFR↓, 1,   HER2/EBBR2↓, 1,   Ki-67↓, 1,   Myc↓, 1,  
Total Targets: 94

Pathway results for Effect on Normal Cells:


Redox & Oxidative Stress ⓘ

antiOx↑, 1,   GSH↑, 1,   GSSG↓, 1,   lipid-P↓, 1,   MDA↓, 1,   NRF2↑, 1,   ROS↓, 2,   SOD↑, 1,  

Core Metabolism/Glycolysis ⓘ

ALAT↓, 1,   cMyc↓, 1,  

Cell Death ⓘ

iNOS↓, 1,  

Proliferation, Differentiation & Cell State ⓘ

mTOR↑, 1,  

Migration ⓘ

MMP2↓, 1,  

Angiogenesis & Vasculature ⓘ

angioG↓, 1,   eNOS↓, 2,   NO↓, 1,   VEGF↓, 1,  

Immune & Inflammatory Signaling ⓘ

COX2↓, 1,   IL6↓, 1,   Inflam↓, 1,   NF-kB↓, 1,   PGE2↓, 1,   TNF-α↓, 1,  

Drug Metabolism & Resistance ⓘ

eff↑, 1,  

Clinical Biomarkers ⓘ

ALAT↓, 1,   AST↓, 1,   IL6↓, 1,  

Functional Outcomes ⓘ

neuroP↑, 2,  
Total Targets: 28

Scientific Paper Hit Count for: eNOS, endothelial Nitric Oxide Synthase
1 Alpha-Lipoic-Acid
1 Apigenin (mainly Parsley)
1 Emodin
1 Fisetin
1 Rosmarinic acid
1 Sulforaphane (mainly Broccoli)
1 Gemcitabine (Gemzar)
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

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