NQO1 Cancer Research Results
NQO1, NAD(P)H quinone dehydrogenase 1: Click to Expand ⟱
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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.
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Scientific Papers found: Click to Expand⟱
OS↑, BBR could sensitize ICB to inhibit tumor growth and increased the survival rate of mice.
ROS↑,
NQO1↓,
ICD↑,
NRF2↓, Brusatol is a potent Nrf2 inhibitor for future cancer treatment.
TumCG↓, Brusatol exhibits significant tumor inhibition in multiple cancers.
ChemoSen↑, also exhibits significant synergistic antitumor effects in combination with chemotherapeutic agents
ROS↑, Graphical Abstract
NF-kB↓,
Akt↓,
mTOR↓,
TumCCA↑,
Apoptosis↑,
PARP↑,
Casp↑,
P53↓,
Bcl-2↓,
PI3K↓,
JAK2↓,
EMT↓,
p27↑,
ROCK1↓,
MMP2↓,
MMP9↓,
NRF2↓, which is the reason why brusatol is called an Nrf2 inhibitor [15]. Brusatol is a potent Nrf2 inhibitor
AntiTum↑, Brusatol shows significant antitumor effects in vitro and in vivo
HO-1↓, Moreover, brusatol inhibited the expression of Nrf2 downstream genes, such as HO-1 [19], [31], [32], NQO1 [43], [44], VEGF [45], and AKR1C1 [46].
NQO1↓,
VEGF↓,
MRP1↓, brusatol reduced both the mRNA and protein levels of NQO1, HO-1, MDR1, and MRP5
RadioS↑, Improvement of sensitivity to radiotherapy and phototherapy
PhotoS↑,
toxicity↝, the toxicity of brusatol is a problem that can not be ignored.
NRF2↓, luteolin inhibited the Nrf2 pathway in oxaliplatin-resistant cell lines in a dose-dependent manner.
NQO1↓, Luteolin also inhibited Nrf2 target gene [NQO1, heme oxygenase-1 (HO-1) and GSTα1/2] expression and decreased reduced glutathione in wild type mouse small intestinal cells.
HO-1↓,
GSH↓,
ChemoSen↑, uteolin combined with other chemotherapeutics had greater anti-cancer activity in resistant cell lines (combined index values below 1), indicating a synergistic effect.
RadioS↑, it can be used as an adjuvant to radio-chemotherapy and helps to ameliorate cancer complications
ChemoSen↑,
chemoP↑,
*lipid-P↓, ↓LPO, ↑CAT, ↑SOD, ↑GPx, ↑GST, ↑GSH, ↓TNF-α, ↓IL-1β, ↓Caspase-3, ↑IL-10
*Catalase↑,
*SOD↑,
*GPx↑,
*GSTs↑,
*GSH↑,
*TNF-α↓,
*IL1β↓,
*Casp3↓,
*IL10↑,
NRF2↓, Lung cancer model ↓Nrf2, ↓HO-1, ↓NQO1, ↓GSH
HO-1↓,
NQO1↓,
GSH↓,
MET↓, Lung cancer model ↓MET, ↓p-MET, ↓p-Akt, ↓HGF
p‑MET↓,
p‑Akt↓,
HGF/c-Met↓,
NF-kB↓, Lung cancer model ↓NF-κB, ↓Bcl-XL, ↓MnSOD, ↑Caspase-8, ↑Caspase-3, ↑PARP
Bcl-2↓,
SOD2↓,
Casp8↑,
Casp3↑,
PARP↑,
MAPK↓, LLC-induced BCP mouse model ↓p38 MAPK, ↓GFAP, ↓IBA1, ↓NLRP3, ↓ASC, ↓Caspase1, ↓IL-1β
NLRP3↓,
ASC↓,
Casp1↓,
IL6↓, Lung cancer model ↓TNF‑α, ↓IL‑6, ↓MuRF1, ↓Atrogin-1, ↓IKKβ, ↓p‑p65, ↓p-p38
IKKα↓,
p‑p65↓,
p‑p38↑,
MMP2↓, Lung cancer model ↓MMP-2, ↓ICAM-1, ↓EGFR, ↓p-PI3K, ↓p-Akt
ICAM-1↓,
EGFR↑,
p‑PI3K↓,
E-cadherin↓, Lung cancer model ↑E-cadherin, ↑ZO-1, ↓N-cadherin, ↓Claudin-1, ↓β-Catenin, ↓Snail, ↓Vimentin, ↓Integrin β1, ↓FAK
ZO-1↑,
N-cadherin↓,
CLDN1↓,
β-catenin/ZEB1↓,
Snail↓,
Vim↑,
ITGB1↓,
FAK↓,
p‑Src↓, Lung cancer model ↓p-FAK, ↓p-Src, ↓Rac1, ↓Cdc42, ↓RhoA
Rac1↓,
Cdc42↓,
Rho↓,
PCNA↓, Lung cancer model ↓Cyclin B1, ↑p21, ↑p-Cdc2, ↓Vimentin, ↓MMP9, ↑E-cadherin, ↓AIM2, ↓Pro-caspase-1, ↓Caspase-1 p10, ↓Pro-IL-1β, ↓IL-1β, ↓PCNA
Tyro3↓, Lung cancer model ↓TAM RTKs, ↓Tyro3, ↓Axl, ↓MerTK, ↑p21
AXL↓,
CEA↓, B(a)P induced lung carcinogenesis ↓CEA, ↓NSE, ↑SOD, ↑CAT, ↑GPx, ↑GR, ↑GST, ↑GSH, ↑Vitamin E, ↑Vitamin C, ↓PCNA, ↓CYP1A1, ↓NF-kB
NSE↓,
SOD↓,
Catalase↓,
GPx↓,
GSR↓,
GSTs↓,
GSH↓,
VitE↓,
VitC↓,
CYP1A1↓,
cFos↑, Lung cancer model ↓Claudin-2, ↑p-ERK1/2, ↑c-Fos
AR↓, ↓Androgen receptor
AIF↑, Lung cancer model ↑Apoptosis-inducing factor protein
p‑STAT6↓, ↓p-STAT6, ↓Arginase-1, ↓MRC1, ↓CCL2
p‑MDM2↓, Lung cancer model ↓p-PI3K, ↓p-Akt, ↓p-MDM2, ↑p-P53, ↓Bcl-2, ↑Bax
NOTCH1↓, Lung cancer model ↑Bax, ↑Cleaved-caspase 3, ↓Bcl2, ↑circ_0000190, ↓miR-130a-3p, ↓Notch-1, ↓Hes-1, ↓VEGF
VEGF↓,
H3↓, Lung cancer model ↑Caspase 3, ↑Caspase 7, ↓H3 and H4 HDAC activities
H4↓,
HDAC↓,
SIRT1↓, Lung cancer model ↑Bax/Bcl-2, ↓Sirt1
ROS↑, Lung cancer model ↓NF-kB, ↑JNK, ↑Caspase 3, ↑PARP, ↑ROS, ↓SOD
DR5↑, Lung cancer model ↑Caspase-8, ↑Caspase-3, ↑Caspase-9, ↑DR5, ↑p-Drp1, ↑Cytochrome c, ↑p-JNK
Cyt‑c↑,
p‑JNK↑,
PTEN↓, Lung cancer model 1/5/10/30/50/80/100 μmol/L ↑Cleaved caspase-3, ↑PARP, ↑Bax, ↓Bcl-2, ↓EGFR, ↓PI3K/Akt/PTEN/mTOR, ↓CD34, ↓PCNA
mTOR↓,
CD34↓,
FasL↑, Lung cancer model ↑DR 4, ↑FasL, ↑Fas receptor, ↑Bax, ↑Bad, ↓Bcl-2, ↑Cytochrome c, ↓XIAP, ↑p-eIF2α, ↑CHOP, ↑p-JNK, ↑LC3II
Fas↑,
XIAP↓,
p‑eIF2α↑,
CHOP↑,
LC3II↑,
PD-1↓, Lung cancer model ↓PD-L1, ↓STAT3, ↑IL-2
STAT3↓,
IL2↑,
EMT↓, Luteolin exerts anticancer activity by inhibiting EMT, and the possible mechanisms include the inhibition of the EGFR-PI3K-AKT and integrin β1-FAK/Src signaling pathways
cachexia↓, luteolin could be a potential safe and efficient alternative therapy for the treatment of cancer cachexi
BioAv↑, A low-energy blend of castor oil, kolliphor and polyethylene glycol 200 increases the solubility of luteolin by a factor of approximately 83
*Half-Life↝, ats administered an intraperitoneal injection of luteolin (60 mg/kg) absorbed it rapidly as well, with peak levels reached at 0.083 h (71.99 ± 11.04 μg/mL) and a prolonged half-life (3.2 ± 0.7 h)
*eff↑, Luteolin chitosan-encapsulated nano-emulsions increase trans-nasal mucosal permeation nearly 6-fold, drug half-life 10-fold, and biodistribution of luteolin in brain tissue 4.4-fold after nasal administration
TumCP↓, PLB inhibited cell proliferation, activated death receptor-mediated apoptotic pathway,
NRF2↓, PLB induces intracellular ROS generation and regulates redox homeostasis via suppressing Nrf2-mediated oxidative signaling pathway in SCC25 cells
TumCCA↑, PLB markedly induced cell cycle arrest at G2/M phase and extrinsic apoptosis
EMT↓, and inhibited epithelial to mesenchymal transition (EMT) and stemness in SCC25 cells.
CSCs↓,
eff↓, Of note, N-acetyl-l-cysteine (NAC) and l-glutathione (GSH) abolished the effects of PLB on cell cycle arrest, apoptosis induction, EMT inhibition, and stemness a
ROS↑, PLB on ROS generation-related molecules
CycB/CCNB1↓, PLB induces G2/M arrest in SCC25 cells via downregulation of cyclin B1, CDK1/cdc2, and cdc25
CDK1↓,
CDK2↓,
CDC25↓,
Vim↓, PLB inhibited the expression of vimentin in a concentration- and time-dependent manner
OCT4↓, PLB significantly decreased the expression level of Oct-4, Sox-2, Nanog, and Bmi-1.
SOX2↓,
Nanog↓,
BMI1↓,
NQO1↓, The expression levels of NQO1, GST, and HSP90 were all markedly decreased
GSTA1↓,
HSP90↓,
toxicity↓, PLB exhibits anticancer activities with minimal side effect in vitro and in vivo,
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in-vitro, |
Pca, |
PC3 |
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in-vitro, |
Pca, |
DU145 |
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GPx↓, significant reduction of GPx, GR and NQO1 enzymatic activity
GSR↓,
NQO1↓,
NRF2↓, Our study revealed the significant effects of sequential treatment with VC + Q on Nrf2 suppression in prostate cancer cells
ROS↑, The level of ROS had significant reduction up to 18% (P ¼ 0.046) when DU145 cells treated with dose no.1 of VC þ Q to compare with the control
Showing Research Papers: 1 to 6 of 6
* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 6
Pathway results for Effect on Cancer / Diseased Cells:
Redox & Oxidative Stress ⓘ
Catalase↓, 1, CYP1A1↓, 1, GPx↓, 2, GSH↓, 3, GSR↓, 2, GSTA1↓, 1, GSTs↓, 1, HO-1↓, 3, ICD↑, 1, NQO1↓, 6, NRF2↓, 6, ROS↑, 5, SOD↓, 1, SOD2↓, 1, VitC↓, 1, VitE↓, 1,
Mitochondria & Bioenergetics ⓘ
AIF↑, 1, CDC25↓, 1, XIAP↓, 1,
Core Metabolism/Glycolysis ⓘ
SIRT1↓, 1,
Cell Death ⓘ
Akt↓, 1, p‑Akt↓, 1, Apoptosis↑, 1, Bcl-2↓, 2, Casp↑, 1, Casp1↓, 1, Casp3↑, 1, Casp8↑, 1, Cyt‑c↑, 1, DR5↑, 1, Fas↑, 1, FasL↑, 1, HGF/c-Met↓, 1, p‑JNK↑, 1, MAPK↓, 1, p‑MDM2↓, 1, p27↑, 1, p‑p38↑, 1,
Transcription & Epigenetics ⓘ
H3↓, 1, H4↓, 1, PhotoS↑, 1,
Protein Folding & ER Stress ⓘ
CHOP↑, 1, p‑eIF2α↑, 1, HSP90↓, 1,
Autophagy & Lysosomes ⓘ
LC3II↑, 1,
DNA Damage & Repair ⓘ
P53↓, 1, PARP↑, 2, PCNA↓, 1,
Cell Cycle & Senescence ⓘ
CDK1↓, 1, CDK2↓, 1, CycB/CCNB1↓, 1, TumCCA↑, 2,
Proliferation, Differentiation & Cell State ⓘ
BMI1↓, 1, CD34↓, 1, cFos↑, 1, CSCs↓, 1, EMT↓, 3, HDAC↓, 1, mTOR↓, 2, Nanog↓, 1, NOTCH1↓, 1, OCT4↓, 1, PI3K↓, 1, p‑PI3K↓, 1, PTEN↓, 1, SOX2↓, 1, p‑Src↓, 1, STAT3↓, 1, p‑STAT6↓, 1, TumCG↓, 1,
Migration ⓘ
AXL↓, 1, Cdc42↓, 1, CEA↓, 1, CLDN1↓, 1, E-cadherin↓, 1, FAK↓, 1, ITGB1↓, 1, MET↓, 1, p‑MET↓, 1, MMP2↓, 2, MMP9↓, 1, N-cadherin↓, 1, Rac1↓, 1, Rho↓, 1, ROCK1↓, 1, Snail↓, 1, TumCP↓, 1, Tyro3↓, 1, Vim↓, 1, Vim↑, 1, ZO-1↑, 1, β-catenin/ZEB1↓, 1,
Angiogenesis & Vasculature ⓘ
EGFR↑, 1, VEGF↓, 2,
Immune & Inflammatory Signaling ⓘ
ASC↓, 1, ICAM-1↓, 1, IKKα↓, 1, IL2↑, 1, IL6↓, 1, JAK2↓, 1, NF-kB↓, 2, p‑p65↓, 1, PD-1↓, 1,
Protein Aggregation ⓘ
NLRP3↓, 1,
Hormonal & Nuclear Receptors ⓘ
AR↓, 1,
Drug Metabolism & Resistance ⓘ
BioAv↑, 1, ChemoSen↑, 3, eff↓, 1, MRP1↓, 1, RadioS↑, 2,
Clinical Biomarkers ⓘ
AR↓, 1, CEA↓, 1, EGFR↑, 1, IL6↓, 1, NSE↓, 1,
Functional Outcomes ⓘ
AntiTum↑, 1, cachexia↓, 1, chemoP↑, 1, OS↑, 1, toxicity↓, 1, toxicity↝, 1,
Total Targets: 121
Pathway results for Effect on Normal Cells:
Redox & Oxidative Stress ⓘ
Catalase↑, 1, GPx↑, 1, GSH↑, 1, GSTs↑, 1, lipid-P↓, 1, SOD↑, 1,
Cell Death ⓘ
Casp3↓, 1,
Immune & Inflammatory Signaling ⓘ
IL10↑, 1, IL1β↓, 1, TNF-α↓, 1,
Drug Metabolism & Resistance ⓘ
eff↑, 1, Half-Life↝, 1,
Total Targets: 12
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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