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⟱
2657- AL,    Allicin pharmacology: Common molecular mechanisms against neuroinflammation and cardiovascular diseases
- Review, CardioV, NA - Review, AD, NA
*Inflam↓, allicin integrate a broad spectrum of properties (e.g., anti-inflammatory, immunomodulatory, antibiotic, antifungal, antiparasitic, antioxidant, nephroprotective, neuroprotective, cardioprotective, and anti-tumoral activities, among others).
*antiOx↑, improving the antioxidant system
*neuroP↑,
*cardioP↑,
*AntiTum↑,
*mtDam↑, Indeed, the current evidence suggests that allicin improves mitochondrial function by enhancing the expression of HSP70 and NRF2, decreasing RAAS activation, and promoting mitochondrial fusion processes.
*HSP70/HSPA5↑, llicin improves mitochondrial function by enhancing the expression of HSP70 and decreasing RAAS activation
*NRF2↑,
*RAAS↓,
*cognitive↑, Allicin enhances the cognitive function of APP (amyloid precursor protein)/PS1 (presenilin 1) double transgenic mice by decreasing the expression levels of Aβ, oxidative stress, and improving mitochondrial function.
*SOD↑, positive effects on cognition in an AD mouse model by administrating a preventive dose of allicin. These effects might be mediated by an increase of SOD and reduction of ROS
*ROS↓,
*NRF2↑, Chronic treatment with allicin increased the expression of NRF2 and targeted downstream of NRF2, such as NADPH, quinone oxidoreductase 1 (NQO1), and γ-glutamyl cysteine synthetase (γ-GCS), in the hippocampus of aged mice
*ER Stress↓, protective effects of 16 weeks of allicin treatment in a rat model of endoplasmic reticulum stress-related cognitive deficits.
*neuroP↑, allicin was able to ameliorate depressive-like behaviors by decreasing neuroinflammation, oxidative stress iron aberrant accumulation,
*memory↑, allicin improved lead acetate-caused learning and memory deficits and decreased the ROS level
*TBARS↓, Oral administration of allicin was able to reduce thiobarbituric reactive substances (TBARS) and myeloperoxidase (MPO) levels, and concurrently increased (SOD) activity, glutathione S-transferase (GST) and glutathione (GSH) levels in a rat model of
*MPO↓,
*SOD↑,
*GSH↑,
*iNOS↓, decreasing the expression of iNOS and increased the phosphorylation of endothelial NOS (eNOS)
*p‑eNOS↑,
*HO-1↑, OSCs upregulate the endogenous antioxidant NRF2 and heme oxygenase-1 (HO-1)

3272- ALA,    Alpha-lipoic acid as a dietary supplement: Molecular mechanisms and therapeutic potential
- Review, AD, NA
*antiOx↑, LA has long been touted as an antioxidant,
*glucose↑, improve glucose and ascorbate handling,
*eNOS↑, increase eNOS activity, activate Phase II detoxification via the transcription factor Nrf2, and lower expression of MMP-9 and VCAM-1 through repression of NF-kappa-B.
*NRF2↑,
*MMP9↓,
*VCAM-1↓,
*NF-kB↓,
*cardioP↑, used to improve age-associated cardiovascular, cognitive, and neuromuscular deficits,
*cognitive↑,
*eff↓, The efficiency of LA uptake was also lowered by its administration in food,
*BBB↑, LA has been shown to cross the blood-brain barrier in a limited number of studies;
*IronCh↑, LA preferentially binds to Cu2+, Zn2+ and Pb2+, but cannot chelate Fe3+, while DHLA forms complexes with Cu2+, Zn2+, Pb2+, Hg2+ and Fe3+
*GSH↑, LA markedly increases intracellular glutathione (GSH),
*PKCδ↑, PKCδ, LA activates Erk1/2 [92,93], p38 MAPK [94], PI3 kinase [94], and Akt
*ERK↑,
*p38↑,
*MAPK↑,
*PI3K↑,
*Akt↑,
*PTEN↓, LA decreases the activities of Protein Tyrosine Phosphatase 1B [99], Protein Phosphatase 2A [95], and the phosphatase and tensin homolog PTEN [95],
*AMPK↑, LA activates peripheral AMPK
*GLUT4↑, stimulate GLUT4 translocation
*GLUT1↑, LA-stimulated translocation of GLUT1 and GLUT4.
*Inflam↓, LA as an anti-inflammatory agent

5834- CAP,    Capsaicin and TRPV1: A Novel Therapeutic Approach to Mitigate Vascular Aging
- Study, Nor, NA
*AntiCan↑, capsaicin possesses anti-cancer, anti-inflammatory, and antioxidant properties and is used as a topical analgesic
*Inflam↓,
*antiOx↑,
*TRPV1↑, Studies demonstrate that capsaicin directly activates TRPV1 by binding to intracellular sites within the channel protein
*AMPK↑, Moreover, capsaicin and TRPV1 can activate the AMPK pathway [82, 83]
*SIRT1↑, elevating SIRT1 levels
*NADPH↓, suppressing NADPH oxidase and reducing reactive oxygen species
*ROS↓,
*MAPK↓, inhibiting MAPK pathways
*eNOS↑, activating eNOS
*Wnt/(β-catenin)↓, inhibiting the Wnt/β-catenin signaling pathway
RenoP↑, Furthermore, TRPV1 activation decreases renal perfusion pressure while increasing glomerular filtration rate and the excretion of sodium/water, thereby modulating renal hemodynamics and excretory functions

4987- Dipy,  ATV,    Enhanced cardioprotection against ischemia-reperfusion injury with a dipyridamole and low-dose atorvastatin combination
- in-vivo, Nor, NA
*cardioP↑, In conclusion, low-dose ATV and DIP had synergistic effects in reducing myocardial IS and activation of Akt and eNOS.
*Akt↑,
*eNOS↑,

1672- PBG,    The Potential Use of Propolis as an Adjunctive Therapy in Breast Cancers
- Review, BC, NA
ChemoSen↓, 4 human clinical trials that demonstrated the successful use of propolis in alleviating side effects of chemotherapy and radiotherapy while increasing the quality of life of breast cancer patients, with minimal adverse effects.
RadioS↑,
Inflam↓, immunomodulatory, anti-inflammatory, and anti-cancer properties.
AntiCan↑,
Dose∅, Indonesia: IC50 = 4.57 μg/mL and 10.23 μg/mL
mtDam↑, Poland: propolis induced mitochondrial damage and subsequent apoptosis in breast cancer cells.
Apoptosis?,
OCR↓, China: CAPE inhibited mitochondrial oxygen consumption rate (OCR) by reducing basal, maximal, and spare respiration rate and consequently inhibiting ATP production
ATP↓,
ROS↑, Iran: inducing intracellular ROS production, IC50 = 65-96 μg/mL
ROS↑, Propolis induced mitochondrial dysfunction and lactate dehydrogenase release indicating the occurrence of ROS-associated necrosis.
LDH↓,
TP53↓, Interestingly, a reduced expression of apoptosis-related genes such as TP53, CASP3, BAX, and P21)
Casp3↓,
BAX↓,
P21↓,
ROS↑, CAPE: inducing oxidative stress through upregulation of e-NOS and i-NOS levels
eNOS↑,
iNOS↑,
eff↑, The combination of propolis and mangostin significantly reduced the expression of Wnt2, FAK, and HIF-1α, when compared to propolis or mangostin alone
hTERT/TERT↓, downregulation of the mRNA levels of hTERT and cyclin D1
cycD1/CCND1↓,
eff↑, Synergism with bee venom was observed
eff↑, Statistically significant decrease was found in the MCF-7 cell viability 48 h after applying different combinations of cisplatin (3.12 μg/mL) and curcumin (0.31 μg/mL) and propolis (160 μg/mL)
eff↑, Nanoparticles of chrysin had significantly higher cytotoxicity against MCF-7 cells, compared to chrysin
eff↑, Propolis nanoparticles appeared to increase cytotoxicity of propolis against MCF-7 cells
STAT3↓, Chrysin also inhibited the hypoxia-induced STAT3 tyrosine phosphorylation suggesting the mechanism of action was through STAT3 inhibition.
TIMP1↓, Propolis reduced the expression of TIMP-1, IL-4, and IL-10.
IL4↓,
IL10↓,
OS↑, patients supplemented with propolis had significantly longer median disease free survival time (400 mg, 3 times daily for 10 d pre-, during, and post)
Dose∅, 400 mg, 3 times daily for 10 d pre-, during, and post
ER Stress↑, endoplasmic reticulum stress
ROS↑, upregulating the expression of Annexin A7 (ANXA7), reactive oxygen species (ROS) level, and NF-κB p65 level, while simultaneously reducing the mitochondrial membrane potential.
NF-kB↓,
p65↓,
MMP↓,
TumAuto↑, propolis induced autophagy by increasing the expression of LC3-II and reducing the expression of p62 level
LC3II↑,
p62↓,
TLR4↓, propolis downregulates the inflammatory TLR4
mtDam↑, propolis induced mitochondrial dysfunction and lactate dehydrogenase release indicating ROS-associated necrosis in MDA MB-231cancer cells
LDH↓,
ROS↑,
Glycolysis↓, inhibit the proliferation of MDA-MB-231 cells by targeting key enzymes of glycolysis, namely glycolysis-hexokinase 2 (HK2), phosphofructokinase (PFK), pyruvate kinase muscle isozyme M2 (PKM2), and lactate dehydrogenase A (LDHA),
HK2↓,
PFK↓,
PKM2↓,
LDH↓,
IL10↓, propolis significantly reduced the relative number of CD4+, CD25+, FoxP3+ regulatory T cells expressing IL-10
HDAC8↓, Chrysin, a propolis bioactive compound, inhibits HDAC8
eff↑, combination of propolis and mangostin significantly reduced the expression of Wnt2, FAK, and HIF-1α, when compared to propolis or mangostin alone.
eff↑, Propolis also upregulated the expression of catalase, HTRA2/Omi, FADD, and TRAIL-associated DR5 and DR4 which significantly enhanced the cytotoxicity of doxorubicin in MCF-7 cells
P21↑, Chrysin, a propolis bioactive compound, inhibits HDAC8 and significantly increases the expression of p21 (waf1/cip1) in breast cancer cells, leading to apoptosis.

2443- RES,    Health Benefits and Molecular Mechanisms of Resveratrol: A Narrative Review
- Review, Var, NA
*antiOx↑, Resveratrol has shown strong antioxidant properties in many studies
*ROS↓,
*PTEN↑, resveratrol upregulated the phosphatase and tensin homolog (PTEN), which decreased Akt phosphorylation, leading to an upregulation of antioxidant enzyme mRNA levels such as catalase (CAT) and superoxide dismutase (SOD)
*Akt↓,
*Catalase↑,
*SOD↑,
*ERK↓, modulating antioxidant enzymes through downregulation of extracellular signal-regulated kinase (ERK)
*GSH↑, thus the levels of antioxidants like glutathione (GSH) increased, and free radicals were directly scavenged
*AMPK↑, resveratrol activated adenosine monophosphate (AMP)-activated protein kinase (AMPK) to maintain the structural stability of forkhead box O1 (FoxO1)
*FOXO1↝,
*RNS↓, Generally, resveratrol protects against oxidative stress mainly by (i) reducing ROS/reactive nitrogen species (RNS) generation; (ii) directly scavenging free radicals; (iii) improving endogenous antioxidant enzymes (e.g., SOD, CAT, and GSH);
*Catalase↑,
*cardioP↑, In summary, the cardiovascular protective effects of resveratrol mainly depend on the capabilities of reducing oxidative stress and alleviating inflammation through Nrf2 and/or SIRT1 activation, PI3K/eNOS upregulation, and NF-κB downregulation.
*PI3K↑,
*eNOS↑,
hepatoP↑, Resveratrol has shown its protective impacts on several liver diseases in some studies

3420- TQ,    Thymoquinone alleviates the accumulation of ROS and pyroptosis and promotes perforator skin flap survival through SIRT1/NF-κB pathway
- in-vitro, Nor, HUVECs - in-vitro, NA, NA
*NF-kB↓, TQ improves perforator flap survival by inhibiting the NF-κB/NLRP3 pathway and promoting angiogenesis.
*NLRP3↓,
*angioG↑,
*MMP9↑, TQ treatment increased the levels of Cadherin-5, MMP9, and VEGF
*VEGF↑,
*OS↑, TQ enhances the survival rate and angiogenesis of multi-regional perforator flaps.
*Pyro?, TQ inhibits pyroptosis after ischemia-reperfusion injury in rat perforator flaps
*ROS↓, TQ ameliorates oxidative stress and apoptosis following ischemia-reperfusion injury in rat perforator flaps
*Apoptosis↓,
*SIRT1↑, Western blot analysis revealed that SIRT1 protein expression increased after TQ treatment,
*SOD1↑, TQ treatment increased the protein expression levels of SOD1, HO1, and eNOS in rat perforator flap tissues, t
*HO-1↑,
*eNOS↑,
*ASC?, In our current experiments, we found that TQ reduced the expression of NLRP3, GSDMD-N, Caspase-1, IL-1β, IL-18, and ASC proteins both in vivo and in vitro.
*Casp1↓,
*IL1β↓,
*IL18↓,

634- VitC,    Intravenous ascorbic acid to prevent and treat cancer-associated sepsis?
- Analysis, NA, NA
other↓, AA may be highly beneficial in addressing cancer-associated inflammation, particularly progression to systemic inflammatory response syndrome (SIRS) and multi organ failure (MOF), has been largely overlooked
iNOS↓,
eNOS↑, AA administration decreases iNOS in the context of inflammation [101,102], but appears to increase eNOS


Showing Research Papers: 1 to 8 of 8

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 8

Pathway results for Effect on Cancer / Diseased Cells:


Redox & Oxidative Stress ⓘ

ROS↑, 5,  

Mitochondria & Bioenergetics ⓘ

ATP↓, 1,   MMP↓, 1,   mtDam↑, 2,   OCR↓, 1,  

Core Metabolism/Glycolysis ⓘ

Glycolysis↓, 1,   HK2↓, 1,   LDH↓, 3,   PFK↓, 1,   PKM2↓, 1,  

Cell Death ⓘ

Apoptosis?, 1,   BAX↓, 1,   Casp3↓, 1,   hTERT/TERT↓, 1,   iNOS↓, 1,   iNOS↑, 1,  

Transcription & Epigenetics ⓘ

other↓, 1,  

Protein Folding & ER Stress ⓘ

ER Stress↑, 1,  

Autophagy & Lysosomes ⓘ

LC3II↑, 1,   p62↓, 1,   TumAuto↑, 1,  

DNA Damage & Repair ⓘ

TP53↓, 1,  

Cell Cycle & Senescence ⓘ

cycD1/CCND1↓, 1,   P21↓, 1,   P21↑, 1,  

Proliferation, Differentiation & Cell State ⓘ

HDAC8↓, 1,   STAT3↓, 1,  

Migration ⓘ

TIMP1↓, 1,  

Angiogenesis & Vasculature ⓘ

eNOS↑, 2,  

Immune & Inflammatory Signaling ⓘ

IL10↓, 2,   IL4↓, 1,   Inflam↓, 1,   NF-kB↓, 1,   p65↓, 1,   TLR4↓, 1,  

Drug Metabolism & Resistance ⓘ

ChemoSen↓, 1,   Dose∅, 2,   eff↑, 7,   RadioS↑, 1,  

Clinical Biomarkers ⓘ

hTERT/TERT↓, 1,   LDH↓, 3,   TP53↓, 1,  

Functional Outcomes ⓘ

AntiCan↑, 1,   hepatoP↑, 1,   OS↑, 1,   RenoP↑, 1,  
Total Targets: 46

Pathway results for Effect on Normal Cells:


Redox & Oxidative Stress ⓘ

antiOx↑, 4,   Catalase↑, 2,   GSH↑, 3,   HO-1↑, 2,   MPO↓, 1,   NRF2↑, 3,   RNS↓, 1,   ROS↓, 4,   SOD↑, 3,   SOD1↑, 1,   TBARS↓, 1,  

Metal & Cofactor Biology ⓘ

IronCh↑, 1,  

Mitochondria & Bioenergetics ⓘ

mtDam↑, 1,  

Core Metabolism/Glycolysis ⓘ

AMPK↑, 3,   glucose↑, 1,   NADPH↓, 1,   SIRT1↑, 2,  

Cell Death ⓘ

Akt↓, 1,   Akt↑, 2,   Apoptosis↓, 1,   Casp1↓, 1,   iNOS↓, 1,   MAPK↓, 1,   MAPK↑, 1,   p38↑, 1,   Pyro?, 1,   TRPV1↑, 1,  

Protein Folding & ER Stress ⓘ

ER Stress↓, 1,   HSP70/HSPA5↑, 1,  

Proliferation, Differentiation & Cell State ⓘ

ERK↓, 1,   ERK↑, 1,   FOXO1↝, 1,   PI3K↑, 2,   PTEN↓, 1,   PTEN↑, 1,   Wnt/(β-catenin)↓, 1,  

Migration ⓘ

MMP9↓, 1,   MMP9↑, 1,   PKCδ↑, 1,   VCAM-1↓, 1,  

Angiogenesis & Vasculature ⓘ

angioG↑, 1,   eNOS↑, 5,   p‑eNOS↑, 1,   VEGF↑, 1,  

Barriers & Transport ⓘ

BBB↑, 1,   GLUT1↑, 1,   GLUT4↑, 1,  

Immune & Inflammatory Signaling ⓘ

ASC?, 1,   IL18↓, 1,   IL1β↓, 1,   Inflam↓, 3,   NF-kB↓, 2,  

Protein Aggregation ⓘ

NLRP3↓, 1,  

Hormonal & Nuclear Receptors ⓘ

RAAS↓, 1,  

Drug Metabolism & Resistance ⓘ

eff↓, 1,  

Functional Outcomes ⓘ

AntiCan↑, 1,   AntiTum↑, 1,   cardioP↑, 4,   cognitive↑, 2,   memory↑, 1,   neuroP↑, 2,   OS↑, 1,  
Total Targets: 62

Scientific Paper Hit Count for: eNOS, endothelial Nitric Oxide Synthase
1 Allicin (mainly Garlic)
1 Alpha-Lipoic-Acid
1 Capsaicin
1 Dipyridamole
1 Atorvastatin
1 Propolis -bee glue
1 Resveratrol
1 Thymoquinone
1 Vitamin C (Ascorbic 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

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