NQO1 Cancer Research Results

NQO1, NAD(P)H quinone dehydrogenase 1: Click to Expand ⟱
Source:
Type:
NQO1 has attracted interest due to its roles in cell defense and marked inducibility during cellular stress. Since NQO1 is highly expressed in many solid tumors, including via upregulation of Nrf2, the design of compounds activated by NQO1 and NQO1-targeted drug delivery have been active areas of research.
NQO1 (NAD(P)H:quinone oxidoreductase 1) is an enzyme that plays a significant role in cellular defense against oxidative stress and the metabolism of various compounds, including quinones and other electrophiles. Its function is crucial in protecting cells from damage caused by reactive oxygen species (ROS) and in the detoxification of potentially harmful substances.
Scientific Papers found: Click to Expand⟱
7765- ISL,    Isoliquiritigenin as a modulator of the Nrf2 signaling pathway: potential therapeutic implications
- Review, Var, NA
*antiOx↑, Isoliquiritigenin (ISL) (PubChem CID:638278) exhibits a diverse range of pharmacological activities, including antioxidant, anticancer, and anti-tumor properties.
*AntiCan↑,
*AntiTum↑,
*AntiDiabetic↑, possess therapeutic effects on various diseases, such as diabetes, cardiovascular diseases, kidney diseases, and cancer, through the activation of the Nrf2 pathway.
*cardioP↑,
*RenoP↑,
*NRF2↑,
*NQO1↝, modulating the expression of antioxidative enzymes such as nicotinamide adenine dinucleotide phosphate quinone oxidoreductase-1(NQO1), heme oxygenase-1 (HO-1), superoxide dismutase (SOD) et al.
*HO-1↑,
*SOD↑,
*toxicity↓, ISL has been widely recognized as a safe phytochemical without any significant toxic, genotoxic, teratogenic properties in treating diseases
*BioAv↓, The research has determined that the bioavailability of ISL in rats following oral administration ranged from 22.70% to 33.62%, indicating a low level of oral bioavailability.
*Half-Life↓, distribution half-life of ISL was found to be 0.3 h, while the elimination half-life for ISL doses of 10, 20, and 50 mg/kg were determined to be 4.9, 4.6, and 4.8 h
*BBB↑, ISL can traverse the blood-brain barriers and exhibit neuroprotective effects in male MCAO-induced focal cerebral ischemic injury
*neuroP↑,
*Stroke↓,
*GSK‐3β↓, he protective effects of ISL have been shown to be exerted through inhibiting GSK-3β activity through increasing the expression levels of phosphorylated (p)-GSK-3β,
*p‑GSK‐3β↑,
*hepatoP↑, ISL has demonstrated its potential as a hepatoprotectant and as a means to mitigate the detrimental impacts of other substances on liver function
*Inflam↓, ISL has demonstrated efficacy in preventing inflammatory bowel disease
*ROS↓, The findings revealed that treatment with ISL effectively reduced the ROS production and attenuated cellular toxicity in RAW.264.7
*MPO↓, ISL has been found to inhibit the production of ROS, myeloperoxidase (MPO), and malondialdehyde (MDA).
*MDA↓,

7780- ISL,    Isoliquiritigenin alleviates LPS/ D-GalN-induced acute liver failure by activating the PGC-1α/ Nrf2 pathway to reduce oxidative stress and inflammatory response
- in-vivo, Nor, NA
*hepatoP↑, ISL significantly improved the liver pathological changes.
*ROS↓, ISL reduced oxidative stress by altering the expression of PGC-1α, Nrf2, HO-1, NQO1, Keap1, GCLC, and GCLM in damaged hepatocytes.
*PGC-1α↝,
*NRF2↑,
*HO-1↑,
*NQO1↝,
*Keap1↝,
*GCLC↝,
*GCLM↝,
*NLRP3↓, NLRP3 inflammasome, IL-1β, IL-6, TNF-α, iNOS, and Mip-2 were repressed by ISL.
*IL1β↓,
*IL6↓,
*TNF-α↓,
*MIP2↓,
*Bax:Bcl2↓, ISL alleviated LPS/D-GalN-induced hepatocytes apoptosis by increasing the Bcl-2/Bax ratio and suppressing the expression of cleaved caspase-3.
*cl‑Casp3↓,
*Inflam↓, ISL improves the ability of anti-oxidative stress, alleviates inflammatory reaction, apoptosis, and inhibits NLRP3 inflammasome
*Apoptosis↓,


Showing Research Papers: 1 to 2 of 2

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 2

Pathway results for Effect on Cancer / Diseased Cells:


Total Targets: 0

Pathway results for Effect on Normal Cells:


NA, unassigned(tgid=0) ⓘ

Stroke↓, 1,  

Redox & Oxidative Stress(tgid=1) ⓘ

antiOx↑, 1,   GCLC↝, 1,   GCLM↝, 1,   HO-1↑, 2,   Keap1↝, 1,   MDA↓, 1,   MPO↓, 1,   NQO1↝, 2,   NRF2↑, 2,   ROS↓, 2,   SOD↑, 1,  

Mitochondria & Bioenergetics(tgid=3) ⓘ

PGC-1α↝, 1,  

Cell Death(tgid=5) ⓘ

Apoptosis↓, 1,   Bax:Bcl2↓, 1,   cl‑Casp3↓, 1,  

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

GSK‐3β↓, 1,   p‑GSK‐3β↑, 1,  

Barriers & Transport(tgid=15) ⓘ

BBB↑, 1,  

Immune & Inflammatory Signaling(tgid=16) ⓘ

IL1β↓, 1,   IL6↓, 1,   Inflam↓, 2,   MIP2↓, 1,   TNF-α↓, 1,  

Protein Aggregation(tgid=19) ⓘ

NLRP3↓, 1,  

Drug Metabolism & Resistance(tgid=21) ⓘ

BioAv↓, 1,   Half-Life↓, 1,  

Clinical Biomarkers(tgid=22) ⓘ

IL6↓, 1,  

Functional Outcomes(tgid=23) ⓘ

AntiCan↑, 1,   AntiDiabetic↑, 1,   AntiTum↑, 1,   cardioP↑, 1,   hepatoP↑, 2,   neuroP↑, 1,   RenoP↑, 1,   toxicity↓, 1,  
Total Targets: 36

Scientific Paper Hit Count for: NQO1, NAD(P)H quinone dehydrogenase 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

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