NO Cancer Research Results

NO, Nitric Oxide: Click to Expand ⟱
Source:
Type:
Once the cancer has begun, NO seems to play a protumoral role rather than antitumoral one as the concentration required to cause tumor cell cytotoxicity cannot be achieved by cancer cells.
The mechanistic roles of nitric oxide (NO) during cancer progression have been important considerations since its discovery as an endogenously generated free radical. Nonetheless, the impacts of this signaling molecule can be seemingly contradictory, being both pro-and antitumorigenic, which complicates the development of cancer treatments based on the modulation of NO fluxes in tumors. At a fundamental level, low levels of NO drive oncogenic pathways, immunosuppression, metastasis, and angiogenesis, while higher levels lead to apoptosis and reduced hypoxia and also sensitize tumors to conventional therapies. However, clinical outcome depends on the type and stage of the tumor as well as the tumor microenvironment.
Nitric oxide is generated by three main nitric oxide synthase isoforms: neuronal (nNOS), endothelial (eNOS), and inducible (iNOS).

– In many cancers, especially under inflammatory conditions, iNOS expression is upregulated. In contrast, eNOS levels may also be altered in cancers such as breast or prostate cancer.

• Expression Patterns in Tumors:
– Elevated iNOS expression is commonly observed in various tumor types (e.g., colon, breast, lung, and melanoma) and is often associated with an inflammatory microenvironment.

– Changes in eNOS and nNOS expression have also been reported and may contribute to angiogenesis and tumor blood flow regulation.
BC, Breast Cancer: Click to Expand ⟱
Breast Cancer
Scientific Papers found: Click to Expand⟱
1603- Cu,  BP,  SDT,    Glutathione Depletion-Induced ROS/NO Generation for Cascade Breast Cancer Therapy and Enhanced Anti-Tumor Immune Response
- in-vitro, BC, 4T1 - in-vivo, NA, NA
GSH↓, Fenton↑, ROS↑, NO↑, sonoS↑, eff↑, NO↑, *toxicity∅, eff?,
2941- PL,    Selective killing of cancer cells by a small molecule targeting the stress response to ROS
- in-vivo, BC, MDA-MB-231 - in-vitro, OS, U2OS - in-vitro, BC, MDA-MB-453
ROS↑, Apoptosis↑, selectivity↑, *ROS∅, GSH↓, GSSG↑, H2O2↑, NO↑, Half-Life?,
2445- SFN,    Sulforaphane-Induced Cell Cycle Arrest and Senescence are accompanied by DNA Hypomethylation and Changes in microRNA Profile in Breast Cancer Cells
- in-vitro, BC, MCF-7 - in-vitro, BC, MDA-MB-231 - in-vitro, BC, SkBr3
TumCCA↑, P21↑, p27↑, NO↑, Akt↓, ATP↓, AMPK↑, TumAuto↑, DNMT1↓, HK2↓, PKM2↓, HDAC3↓, HDAC4↓, HDAC8↓,
1928- TQ,    Thymoquinone Crosstalks with DR5 to Sensitize TRAIL Resistance and Stimulate ROS-Mediated Cancer Apoptosis
- in-vitro, BC, MCF-7 - in-vitro, BC, MDA-MB-231
TumCP↓, DR4↑, DR5↑, Casp8↑, FADD↑, Bcl-2↓, ROS↑, NO↑, MDA↑,
2350- UA,    Ursolic acid-mediated changes in glycolytic pathway promote cytotoxic autophagy and apoptosis in phenotypically different breast cancer cells
- in-vitro, BC, MCF-7 - in-vitro, BC, MDA-MB-231
Akt↓, Glycolysis↓, HK2↓, PKM2↓, ATP↓, lactateProd↓, AMPK↑, TumAuto↑, Apoptosis↑, ERK↓, MMP↓, NO↑, ROS↑, DNAdam↑,

Showing Research Papers: 1 to 5 of 5

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 5

Pathway results for Effect on Cancer / Diseased Cells:


Redox & Oxidative Stress ⓘ

Fenton↑, 1,   GSH↓, 2,   GSSG↑, 1,   H2O2↑, 1,   MDA↑, 1,   ROS↑, 4,  

Mitochondria & Bioenergetics ⓘ

ATP↓, 2,   MMP↓, 1,  

Core Metabolism/Glycolysis ⓘ

AMPK↑, 2,   Glycolysis↓, 1,   HK2↓, 2,   lactateProd↓, 1,   PKM2↓, 2,  

Cell Death ⓘ

Akt↓, 2,   Apoptosis↑, 2,   Bcl-2↓, 1,   Casp8↑, 1,   DR4↑, 1,   DR5↑, 1,   FADD↑, 1,   p27↑, 1,  

Transcription & Epigenetics ⓘ

sonoS↑, 1,  

Autophagy & Lysosomes ⓘ

TumAuto↑, 2,  

DNA Damage & Repair ⓘ

DNAdam↑, 1,   DNMT1↓, 1,  

Cell Cycle & Senescence ⓘ

P21↑, 1,   TumCCA↑, 1,  

Proliferation, Differentiation & Cell State ⓘ

ERK↓, 1,   HDAC3↓, 1,   HDAC4↓, 1,   HDAC8↓, 1,  

Migration ⓘ

TumCP↓, 1,  

Angiogenesis & Vasculature ⓘ

NO↑, 6,  

Drug Metabolism & Resistance ⓘ

eff?, 1,   eff↑, 1,   Half-Life?, 1,   selectivity↑, 1,  
Total Targets: 37

Pathway results for Effect on Normal Cells:


Redox & Oxidative Stress ⓘ

ROS∅, 1,  

Functional Outcomes ⓘ

toxicity∅, 1,  
Total Targets: 2

Scientific Paper Hit Count for: NO, Nitric Oxide
1 Copper and Cu NanoParticles
1 Black phosphorus
1 SonoDynamic Therapy UltraSound
1 Piperlongumine
1 Sulforaphane (mainly Broccoli)
1 Thymoquinone
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:4  Cells:%  prod#:%  Target#:563  State#:%  Dir#:2
  wNotes=0  sortOrder:rid,rpid

 

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