NOX2 Cancer Research Results

NOX2, NADPH Oxidase 2: Click to Expand ⟱
Source:
Type:

NOX2 - NADPH Oxidase 2 / Cytochrome b-245 Beta Chain

Abbreviation: NOX2, CYBB, gp91phox

Type: NADPH oxidase / reactive oxygen species-generating enzyme

Function: NOX2 is the catalytic membrane subunit of the phagocytic NADPH oxidase complex and generates superoxide during immune and inflammatory responses. It is highly expressed in neutrophils, macrophages, and microglia and regulates antimicrobial defense, redox signaling, inflammation, vascular function, and cellular responses to injury.

Cancer: ↑ Increased NOX2 activity within tumor cells and particularly tumor-associated immune cells can promote ROS-dependent survival signaling, inflammation, immune suppression, angiogenesis, invasion, and tumor progression. NOX2-derived ROS from tumor-associated macrophages and other myeloid cells can suppress antitumor lymphocyte function.

Alzheimer's Disease: ↑ Increased and overactivated NOX2 is strongly implicated in Alzheimer's disease. Aβ stimulates microglial NOX2 activity, increasing ROS production, oxidative stress, neuroinflammation, cerebrovascular dysfunction, and neuronal injury. NOX2 inhibition or genetic deletion reduces oxidative and cognitive abnormalities in experimental Alzheimer's disease models.
Scientific Papers found: Click to Expand⟱
7563- HYP,    Hyperoside alleviates macrophages and microglia-mediated neuroinflammation and oxidative stress through activating PI3K/AKT and Nrf2/HO-1 signaling pathway post spinal cord injury
- vitro+vivo, Nor, NA
*Inflam↓, Hyperoside (HYP), a bioactive flavonoid derived from traditional Chinese medicinal herbs, exhibits potent anti-inflammatory and antioxidant properties.
*antiOx↑,
*Dose↝, SCI mice were treated with HYP (10 mg/kg or 50 mg/kg) via intraperitoneal injection
*IL1β↓, HYP treatment significantly reduced the expression of pro-inflammatory mediators (IL-1β, IL-6, TNF-α, iNOS, and COX-2) and oxidative stress-related markers (NOX1, NOX2, and NOX4).
*IL6↓,
*TNF-α↓,
*iNOS↓,
*COX2/PTGS2↓,
*NOX4↓,
*NOX2↓,
*NOX1↓,
*PI3K↑, HYP enhanced the activation of the phosphatidylinositol 3-kinase (PI3K)/protein kinase B (AKT) pathway and upregulated the expression of nuclear factor erythroid 2-related factor 2 (Nrf2) and heme oxygenase-1 (HO-1)
*Akt↑,
*NRF2↑,
*HO-1↑,
*neuroP↑, our findings demonstrate that HYP confers neuroprotection by alleviating neural tissue damage and facilitating locomotor recovery after SCI

7837- ISQ,    Isoquercitrin Delays Denervated Soleus Muscle Atrophy by Inhibiting Oxidative Stress and Inflammation
- in-vivo, Nor, NA
*Dose↝, Isoquercitrin demonstrated the optimal protective effect at 20 mg/kg/d, which was the dose used in subsequent experiments.
*autophagy↓, Following isoquercitrin treatment, mitochondrial vacuolation and autophagy were inhibited, as evidenced by reduced level of autophagy-related proteins (ATG7, BNIP3, LC3B, and PINK1);
*ATG7↓,
*BNIP3↓,
*LC3B↓,
*PINK1↓,
*ROS↓, (ROS) in the target muscle was reduced, which might be associated with the upregulation of antioxidant factors (SOD1, SOD2, NRF2, NQO1, and HO1) and the downregulation of ROS production-related factors (Nox2, Nox4, and DUOX1).
*SOD1↑,
*SOD2↑,
*NRF2↑,
*NQO1↑,
*HO-1↑,
*NOX2↓,
*NOX4↓,
*DUOX1↓,
*IL1β↓, isoquercitrin treatment reduced the levels of inflammatory factors—interleukin (IL)-1β, IL-6, and tumor necrosis factor-α (TNF-α)—in the target muscle and inactivated the JAK/STAT3 signaling pathway.
*IL6↓,
*TNF-α↓,
*JAK↓,
*STAT3↓,
*Inflam↓, via inhibition of oxidative stress and inflammatory response.

7904- IVT,    Isovitexin alleviates myocardial oxidative stress injury in diabetic mice by enhancing myocardial SIRT3 expression and reducing oxidative stress
- in-vivo, Nor, NA
*cardioP↑, ISO treatment of the diabetic mice significantly reduced myocardial inflammatory cell infiltration, lowered the levels of IL-1β, IL-6 and TNF‑α, restored the protein levels of NQO1, NRF2 and SIRT3, and decreased the protein levels of NOX2 and AC-
*IL1β↓,
*IL6↓,
*TNF-α↓,
*NQO1↑,
*NRF2↑,
*SIRT3↑,
*NOX2↓, and decreased the protein levels of NOX2 and AC-SOD2.
*ROS↓, ISO can alleviate diabetic myocardial injury in mice by promoting SIRT3 expression and reducing oxidative stress.


Showing Research Papers: 1 to 3 of 3

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 3

Pathway results for Effect on Cancer / Diseased Cells:


Total Targets: 0

Pathway results for Effect on Normal Cells:


NA, unassigned(tgid=0) ⓘ

autophagy↓, 1,   DUOX1↓, 1,   NOX1↓, 1,   NOX2↓, 3,  

Redox & Oxidative Stress(tgid=1) ⓘ

antiOx↑, 1,   HO-1↑, 2,   NOX4↓, 2,   NQO1↑, 2,   NRF2↑, 3,   ROS↓, 2,   SIRT3↑, 1,   SOD1↑, 1,   SOD2↑, 1,  

Mitochondria & Bioenergetics(tgid=3) ⓘ

PINK1↓, 1,  

Core Metabolism/Glycolysis(tgid=4) ⓘ

ATG7↓, 1,  

Cell Death(tgid=5) ⓘ

Akt↑, 1,   iNOS↓, 1,  

Autophagy & Lysosomes(tgid=9) ⓘ

BNIP3↓, 1,   LC3B↓, 1,  

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

PI3K↑, 1,   STAT3↓, 1,  

Immune & Inflammatory Signaling(tgid=16) ⓘ

COX2/PTGS2↓, 1,   IL1β↓, 3,   IL6↓, 3,   Inflam↓, 2,   JAK↓, 1,   TNF-α↓, 3,  

Drug Metabolism & Resistance(tgid=21) ⓘ

Dose↝, 2,  

Clinical Biomarkers(tgid=22) ⓘ

IL6↓, 3,  

Functional Outcomes(tgid=23) ⓘ

cardioP↑, 1,   neuroP↑, 1,  
Total Targets: 31

Scientific Paper Hit Count for: NOX2, NADPH Oxidase 2
1 Hyperoside
1 isoquercitrin
1 Isovitexin
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#:1660  State#:%  Dir#:1
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