DUOX1 Cancer Research Results

DUOX1, Dual Oxidase 1: Click to Expand ⟱
Source:
Type:

DUOX1 - Dual Oxidase 1

Type: NADPH oxidase / hydrogen peroxide-generating oxidoreductase

Function: DUOX1 is a member of the NADPH oxidase family that generates hydrogen peroxide (H2O2) in response to calcium-dependent activation. It is expressed prominently in epithelial tissues and contributes to redox signaling, mucosal host defense, wound repair, epithelial differentiation, cell migration, and innate immune responses. Functional DUOX1 activity requires the maturation factor DUOXA1.

Cancer: ↓ Frequently reduced or epigenetically silenced in several epithelial cancers, including lung, hepatocellular, and breast cancers, often through DUOX1 promoter hypermethylation. Loss of DUOX1 can promote epithelial-mesenchymal transition, migration, invasion, and impaired antitumor immune signaling, while restoration of DUOX1 can induce cell-cycle arrest and suppress malignant behavior. However, DUOX1-generated H2O2 can promote proliferation, migration, or angiogenesis in selected cancers, making its role partially context-dependent.
Scientific Papers found: Click to Expand⟱
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.


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:


Total Targets: 0

Pathway results for Effect on Normal Cells:


NA, unassigned(tgid=0) ⓘ

autophagy↓, 1,   DUOX1↓, 1,   NOX2↓, 1,  

Redox & Oxidative Stress(tgid=1) ⓘ

HO-1↑, 1,   NOX4↓, 1,   NQO1↑, 1,   NRF2↑, 1,   ROS↓, 1,   SOD1↑, 1,   SOD2↑, 1,  

Mitochondria & Bioenergetics(tgid=3) ⓘ

PINK1↓, 1,  

Core Metabolism/Glycolysis(tgid=4) ⓘ

ATG7↓, 1,  

Autophagy & Lysosomes(tgid=9) ⓘ

BNIP3↓, 1,   LC3B↓, 1,  

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

STAT3↓, 1,  

Immune & Inflammatory Signaling(tgid=16) ⓘ

IL1β↓, 1,   IL6↓, 1,   Inflam↓, 1,   JAK↓, 1,   TNF-α↓, 1,  

Drug Metabolism & Resistance(tgid=21) ⓘ

Dose↝, 1,  

Clinical Biomarkers(tgid=22) ⓘ

IL6↓, 1,  
Total Targets: 22

Scientific Paper Hit Count for: DUOX1, Dual Oxidase 1
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#:1712  State#:%  Dir#:1
  wNotes=on  sortOrder:rid,rpid

 

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