XO Cancer Research Results

XO, xanthine oxidase: Click to Expand ⟱
Source:
Type:
xanthine oxidase The relationship between XO (xanthine oxidase) and Alzheimer’s disease (AD) is an emerging topic in neurodegenerative research, mainly because of XO's role in oxidative stress and inflammation, which are both key features in AD pathology.
-Studies suggest oxidative stress from XO may increase Aβ aggregation and promote tau phosphorylation, both critical to AD progression.
Scientific Papers found: Click to Expand⟱
6557- BSB,    Alpha-bisabolol protects against neonatal asthma by suppressing airway inflammatory signaling
- in-vivo, Nor, NA
*ROS↓, AB significantly decreased mucous gland hypertrophy, eosinophil infiltration, and oxidative stress marker levels in the allergic airway inflammation-induced AB-pretreated rats.
*Inflam↓, AB pretreatment significantly reduced the levels of proinflammatory cytokines, such as interleukin (IL)-1β, IL-6, IL-8, IL-17, monocyte chemoattractant protein-1, C-X-C chemokine receptor type 4 (CXCR4), and thymic stromal lymphopoietin, which were i
*IL1β↓,
*IL6↓,
*IL8↓,
*IL17↓,
*CXCR4↓,
*COX2↓, transcription of cyclooxygenase-2, tumor necrosis factor-α, CXCR4, toll-like receptor 4, Eotaxin-1, and regulated upon activation normal T cell expressed and secreted were significantly suppressed in allergic airway inflammation-induced AB-pretreated
*TLR4↓,
*NO↓, NO, PCO, MDA, and XO, all of these oxidative stress parameters were significantly attenuated in AB-treated allergic airway inflammation-induced rat pups
*MDA↓,
*XO↓,

6216- CUR,    Role of Turmeric and Curcumin in Prevention and Treatment of Chronic Diseases: Lessons Learned from Clinical Trials
- Review, Var, NA
TumCG↓, Curcumin can prevent tumor growth, angiogenesis, epithelial–mesenchymal transition, invasion, and metastasis by modulating the expression of tumor-related non-coding RNA (ncRNA)
angioG↓,
EMT↓,
TumCI↓,
TumMeta↓,
*GutMicro↑, curcumin plays a crucial role in regulating the gut microbiota via biotransformation of curcumin and its metabolites.
*BioAv↓, one of the primary drawbacks of taking curcumin alone is its low bioavailability, which appears to be caused by poor absorption, fast metabolism, and excretion
*HO-1↑, Curcumin is an efficient inducer of hemoxygenase-1 and a powerful inhibitor of reactive oxygen-generating enzymes, such as cyclooxygenase (COX), inducible nitric oxygen synthase (iNOS), lipoxygenase, and xanthine dehydrogenase/oxidase
*ROS↓,
*COX2↓,
*iNOS↓,
PKCδ↓, Curcumin is also a powerful inhibitor of protein kinase C (PKC), tyrosine kinase, epidermal growth factor receptor (EGFR), and IB kinase.
EGFR↓,
NF-kB↓, It suppresses NF-κB activation and the expression of oncogenes, such as c-jun, c-fos, c-myc, Akt, PI3K, cyclin-dependent kinase (CDK)
cJun↓,
cFos↓,
cMyc↓,
Akt↓,
PI3K↓,
CDK4↓,
*TNF-α↓, Continuous supplementation with nanocurcumin (two 40 mg capsules/day after a meal) for 3 months suppressed expression of inflammatory tumor necrosis factor-alpha (TNF-α), high sensitive protein with C-reactive protein (CRP), and interleukin-6 (IL-6)
*CRP↓,
*IL6↓,
MMP9↓, curcumin suppressed metastasis to the lung by suppressing NF-κB, MMP-9, COX-2, and vascular endothelial growth factor (VEGF) expression.
VEGF↓,
JAK↓, Curcumin remarkably inhibits JAK/STAT signaling by downregulating pro-inflammatory interleukins, such as IL-1, IL-2, IL-6, IL-8, IL-12, and MCP-1.
STAT↓,
IL1↓,
IL2↓,
IL6↓,
IL8↓,
IL12↓,
MCP1↓,
Apoptosis↑, It promotes apoptosis and ER stress by targeting phosphorylated protein kinase-like ER-resident kinase,
ER Stress↑,
5LO↓, inhibiting lipoxygenase and xanthine oxidase activity
XO↓,
*NRF2↑, The expression of nuclear factors erythroid 2-related factor (Nrf2) and heme oxygenase 1 (HO-1) is boosted by curcumin
*HO-1↑,
*AChE↓, Curcumin also inhibits the key enzyme acetylcholinesterase (AChE) and p300, a positive regulator of the Wnt/β-catenin pathway
*neuroP↑, Curcumin has also been suggested to prevent and cure neurotoxicity by replenishing dopamine and 3,4-dihydroxyphenylacetic acid levels.
*glucose↓, remarkably lowers blood glucose levels and improves insulin resistance by reducing hepatic glucose synthesis, inhibiting inflammatory reactions produced by hyperglycemia,
*GLUT2↑, boosting glucose transporters 2 (GLUT2), 3 (GLUT3), and 4 (GLUT4) gene expression, enhancing glucose uptake, and activating the AMPK signaling pathway.
*GLUT3↑,
*GLUT4↑,
*GlucoseCon↑,
*AMPK↑,
*BMD↑, Supplementation with nanomicelle curcumin (80 mg) alone or in combination with Nigella sativa oil (1000 mg) for 2–6 months increased plasma levels of miRNA-21 in postmenopausal women with low bone mass density.
*MDA↓, (1000 mg/day) for 8 weeks reduced serum levels of malondialdehyde (MDA) and high-sensitivity CRP (hs-CRP) and increased the total antioxidant capacity in 81 healthy postmenopausal women
*eff↑, Loriczova et al. demonstrated that iron (18 mg and 65 mg) supplementation along with curcumin (500 mg) reduces iron-induced systemic inflammation by reducing plasma levels of TNF-α
eff↑, high-dose vitamin C (25–100 g/day) along with oral nutrient supplementation including curcumin (1–3 g/day) had improved QoL and survival
P53↑, Curcumin was also reported to induce p53 and Bax expression in patients with colorectal cancer, causing apoptosis and DNA fragmentation and suppressing TNF-α and Bcl-2.
BAX↑,
DNAdam↑,
Bcl-2↓,
CSCs↓, The combination of curcumin, 5-fluorouracil (5-FU) and oxaliplatin (FOLFOX) in colorectal liver metastases reduced stem cell markers, such as aldehyde dehydrogenase and CD133.
ALDH↓,
CD133↑,

3713- FA,    Protective Effect of Ferulic Acid on Acetylcholinesterase and Amyloid Beta Peptide Plaque Formation in Alzheimer’s Disease: An In Vitro Study
- Review, AD, NA
*AChE↓, FA has the potential to be an AChE inhibitor, thus helping in blocking the activity of AChE and also reducing the incidence of amyloid beta plaque formation.
*antiOx↑, significant antioxidant property
*neuroP↑, FA has significant antioxidant and neuroprotective effects
*Aβ↓,
*MMP↓, restore mitochondrial membrane potential
*XO↓, FA, at concentrations ranging from 10 Inline graphicM to 320 Inline graphicM, demonstrated substantial inhibition of XO,
*SOD↑, FA has demonstrated the restoration of SOD activity, mitigated lipid peroxidation, and exhibited free radical scavenging capabilities
*lipid-P↑,
*ROS↓,

6562- Ger,    Potential Effects of Geraniol on Cancer and Inflammation-Related Diseases: A Review of the Recent Research Findings
- Review, Var, NA - Review, AD, NA
*Inflam↓, wide spectrum of pharmacological activities including anti-inflammatory, anticancer, antimicrobial, antioxidant, and neuroprotective activities.
*AntiCan↑,
*AntiBio↑,
*antiOx↑,
*neuroP↑,
ROS↓, GNL scavenges free radicals and preserves the activity of antioxidant enzymes.
Apoptosis↑, GNL induces apoptosis and cell cycle arrest, modulates multiple molecular targets, including p53 and STAT3, activates caspases, and modulates inflammation via transcriptional regulation.
TumCCA↑,
P53↝,
STAT3↓, GNL reduces survivin protein levels by downregulating phosphorylated STAT3.
Casp↝,
*Catalase↑, This compound protects various antioxidant enzymes, such as catalase, glutathione-S-transferase, and glutathione peroxidase.
*GSTs↑,
*GPx↑,
*AChE↓, In addition, GNL suppressed acetylcholinesterase (AChE) activity and alleviated oxidative stress by boosting neuronal reduced glutathione (GSH), catalase (CAT), glutathione-S-transferase (GST), and superoxide dismutase (SOD) activities.
*GSH↑,
*SOD↑,
*TBARS↓, It lowered malondialdehyde concentration (TBARS), nitric oxide (NO), and xanthine oxidase (XO), and restored the structural damage to the brain tissue caused by HFD.
*NO↓,
*XO↓,
*memory↑, GNL boosted learning and memory function and ameliorated the inflammation status in the brain by lowering the protein levels of IL-1β, iNOS, NF-κBp65, and COX-2
*IL1β↓,
*iNOS↓,
*NF-kB↓,
*COX2↓,
*NRF2↑, GNL administration ameliorated renal function, alleviated histological changes, and enhanced Nrf-2/HO-1/NQO-1 with a subsequent intensification of antioxidant enzyme activities.
*HO-1↑,
*survivin↓, GNL reduces survivin protein levels by downregulating phosphorylated STAT3.
TumCP↓, They have shown that GNL treatment significantly suppressed oral squamous cell carcinoma (OSCC) cell proliferation and migration in vitro and tumor growth in vivo in a time- and dose-dependent manner.
TumCMig↓,
TumCG↑,
selectivity↑, GNL may be helpful in treating different types of malignancy, while having limited effects on normal cells.
TumMeta↓, GNL has been reported to inhibit cancer metastasis and angiogenesis.
angioG↓,
Hif1a↓, A549 lung cancer cells treated with GNL, downregulation of HIF-1alpha, a VEGF regulator, occurred
Beclin-1↓, GNL also decreases autophagy through downregulation of BNIP3 and beclin-1 expression, which increases apoptotic cell death through HIF-1α signaling.


Showing Research Papers: 1 to 4 of 4

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 4

Pathway results for Effect on Cancer / Diseased Cells:


Redox & Oxidative Stress(tgid=1) ⓘ

ROS↓, 1,  

Core Metabolism/Glycolysis(tgid=4) ⓘ

cMyc↓, 1,  

Cell Death(tgid=5) ⓘ

Akt↓, 1,   Apoptosis↑, 2,   BAX↑, 1,   Bcl-2↓, 1,   Casp↝, 1,  

Transcription & Epigenetics(tgid=7) ⓘ

cJun↓, 1,  

Protein Folding & ER Stress(tgid=8) ⓘ

ER Stress↑, 1,  

Autophagy & Lysosomes(tgid=9) ⓘ

Beclin-1↓, 1,  

DNA Damage & Repair(tgid=10) ⓘ

DNAdam↑, 1,   P53↑, 1,   P53↝, 1,  

Cell Cycle & Senescence(tgid=11) ⓘ

CDK4↓, 1,   TumCCA↑, 1,  

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

ALDH↓, 1,   CD133↑, 1,   cFos↓, 1,   CSCs↓, 1,   EMT↓, 1,   PI3K↓, 1,   STAT↓, 1,   STAT3↓, 1,   TumCG↓, 1,   TumCG↑, 1,  

Migration(tgid=13) ⓘ

5LO↓, 1,   MMP9↓, 1,   PKCδ↓, 1,   TumCI↓, 1,   TumCMig↓, 1,   TumCP↓, 1,   TumMeta↓, 2,  

Angiogenesis & Vasculature(tgid=14) ⓘ

angioG↓, 2,   EGFR↓, 1,   Hif1a↓, 1,   VEGF↓, 1,  

Immune & Inflammatory Signaling(tgid=16) ⓘ

IL1↓, 1,   IL12↓, 1,   IL2↓, 1,   IL6↓, 1,   IL8↓, 1,   JAK↓, 1,   MCP1↓, 1,   NF-kB↓, 1,  

Protein Aggregation(tgid=19) ⓘ

XO↓, 1,  

Drug Metabolism & Resistance(tgid=21) ⓘ

eff↑, 1,   selectivity↑, 1,  

Clinical Biomarkers(tgid=22) ⓘ

EGFR↓, 1,   IL6↓, 1,  
Total Targets: 49

Pathway results for Effect on Normal Cells:


NA, unassigned(tgid=0) ⓘ

AntiBio↑, 1,  

Redox & Oxidative Stress(tgid=1) ⓘ

antiOx↑, 2,   Catalase↑, 1,   GPx↑, 1,   GSH↑, 1,   GSTs↑, 1,   HO-1↑, 3,   lipid-P↑, 1,   MDA↓, 2,   NRF2↑, 2,   ROS↓, 3,   SOD↑, 2,   TBARS↓, 1,  

Mitochondria & Bioenergetics(tgid=3) ⓘ

MMP↓, 1,  

Core Metabolism/Glycolysis(tgid=4) ⓘ

AMPK↑, 1,   glucose↓, 1,   GlucoseCon↑, 1,   GLUT2↑, 1,  

Cell Death(tgid=5) ⓘ

iNOS↓, 2,   survivin↓, 1,  

Angiogenesis & Vasculature(tgid=14) ⓘ

NO↓, 2,  

Barriers & Transport(tgid=15) ⓘ

GLUT3↑, 1,   GLUT4↑, 1,  

Immune & Inflammatory Signaling(tgid=16) ⓘ

COX2↓, 3,   CRP↓, 1,   CXCR4↓, 1,   IL17↓, 1,   IL1β↓, 2,   IL6↓, 2,   IL8↓, 1,   Inflam↓, 2,   NF-kB↓, 1,   TLR4↓, 1,   TNF-α↓, 1,  

Synaptic & Neurotransmission(tgid=18) ⓘ

AChE↓, 3,  

Protein Aggregation(tgid=19) ⓘ

Aβ↓, 1,   XO↓, 3,  

Drug Metabolism & Resistance(tgid=21) ⓘ

BioAv↓, 1,   eff↑, 1,  

Clinical Biomarkers(tgid=22) ⓘ

BMD↑, 1,   CRP↓, 1,   GutMicro↑, 1,   IL6↓, 2,  

Functional Outcomes(tgid=23) ⓘ

AntiCan↑, 1,   memory↑, 1,   neuroP↑, 3,  
Total Targets: 46

Scientific Paper Hit Count for: XO, xanthine oxidase
1 α-Bisabolol / Chamomile oil
1 Curcumin
1 Ferulic acid
1 Geraniol
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#:1353  State#:%  Dir#:1
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