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.
Pca, Prostate Cancer: Click to Expand ⟱
Prostate Cancer: Alterations in genes such as ERG, SPOP, MYC, androgen receptor (AR), and CHD1, drive PCa progression.
TP53 is the most commonly mutated gene in human cancer.
HH↑, GLI-1↑, SHH↑ P53↓
The loss of p53 and/or other tumor suppressor genes, reduced capacity for DNA repair, the dysfunction of telomerase activity, and changes in the pathways that govern the growth of cells also mediate the progression of Pca.
It has been well documented that Ca2+ influx and MDR1 upregulation are highly associated with GEM metabolism in human pancreatic carcinoma.
Increased Growth factor IGF-1/IGF-1R axis activation mediated by both PI3K/Akt or RAF/MEK/ERK system and AR expression remains important in the development and progression of prostate cancer.
It has been demonstrated that prostate cancer cells are relatively sensitive to heat stress.
Long non-coding RNA MALAT1 has been reported as an oncogenic target in multiple types of cancers, including PC.
Scientific Papers found: Click to Expand⟱
7691- IP6,    Inositol Hexaphosphate Suppresses Growth and Induces Apoptosis in Prostate Carcinoma Cells in Culture and Nude Mouse Xenograft: PI3K-Akt Pathway as Potential Target
- vitro+vivo, Pca, PC3 - in-vitro, Pca, C4-2B
TumCP↓, Apoptosis↑, Casp3↑, cl‑PARP↑, Akt↓, PI3K↓, p‑GSK‐3β↓, cycD1/CCND1↓, TumVol↓, TumW↓, PCNA↓, angioG↓, CD31/PECAM-1↓, ILK↓, VEGF↓, eNOS↓, Hif1a↓,

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:


NA, unassigned(tgid=0) ⓘ

ILK↓, 1,  

Cell Death(tgid=5) ⓘ

Akt↓, 1,   Apoptosis↑, 1,   Casp3↑, 1,  

DNA Damage & Repair(tgid=10) ⓘ

cl‑PARP↑, 1,   PCNA↓, 1,  

Cell Cycle & Senescence(tgid=11) ⓘ

cycD1/CCND1↓, 1,  

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

p‑GSK‐3β↓, 1,   PI3K↓, 1,  

Migration(tgid=13) ⓘ

CD31/PECAM-1↓, 1,   TumCP↓, 1,  

Angiogenesis & Vasculature(tgid=14) ⓘ

angioG↓, 1,   eNOS↓, 1,   Hif1a↓, 1,   VEGF↓, 1,  

Functional Outcomes(tgid=23) ⓘ

TumVol↓, 1,   TumW↓, 1,  
Total Targets: 17

Pathway results for Effect on Normal Cells:


Total Targets: 0

Scientific Paper Hit Count for: eNOS, endothelial Nitric Oxide Synthase
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:22  Cells:%  prod#:%  Target#:820  State#:%  Dir#:1
  wNotes=0  sortOrder:rid,rpid

 

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