NLRP3 Cancer Research Results
NLRP3, NOD-like receptor pyrin domain-containing protein 3: Click to Expand ⟱
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NLRP3 (NOD-like receptor pyrin domain-containing protein 3) is a protein that plays a crucial role in the regulation of inflammation and immune responses.
NLRP3 typically has high expression in cancers, with poor prognosis.
For alzheimer's disease:
-NLRP3 is upregulated in Alzheimer's disease (AD)
-NLRP3 is activated in microglia in response to amyloid-β (Aβ) and tau aggregates.
-Promotes tau hyperphosphorylation and spread via inflammation-driven pathways.
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Scientific Papers found: Click to Expand⟱
TumAuto↑, Overall, 10-nm AgNPs showed the highest cellular responses compared with 50- and 100-nm AgNPs . autophagy-lysosomal system
EPR↑, 10-nm AgNPs exhibited the highest uptake and accumulation.
LC3B↑, Subcytotoxic concentrations of AgNPs enhanced expression of LC3B, a pro-autophagic protein, and CHOP, an apoptosis inducing ER-stress protein, and activation of NLRP3-inflammasome (caspase-1, IL-1β).
CHOP↑,
ER Stress↑,
NLRP3↑,
Casp1↓,
DDS↑, various biomedical applications, including drug delivery, cartilage repair, wound healing, and tissue engineering, because of its unique physicochemical properties.
*Cartilage↑,
*Wound Healing↑,
Imm↑, investigation of the immunomodulatory properties of chitosan, since the biopolymer has been shown to modulate the maturation, activation, cytokine production, and polarization of dendritic cells and macrophages
cGAS–STING↑, Several signaling pathways, including the cGAS–STING, STAT-1, and NLRP3 inflammasomes, are involved in chitosan-induced immunomodulation. CS activates the cGAS–STING signaling pathway
STAT1↑, One crucial factor is DDA, as it was observed that 80% DDA CS activated the STAT-1 pathway, whereas 98% DDA did not
NLRP3↑, activation of the NLRP3 inflammasome by CS requires the presence of mitochondrial ROS.
*DCells↑, CS has been studied for its potential impact on DC activation, which is a crucial step in initiating the immune response.
*IL10↓, The use of CS also reduced IL-10 production and increased TGF-β1, TNF-α, and interleukin-1 beta (IL-1β) (p < 0.001) levels.
*TGF-β1↓,
*TNF-α↓,
IL1β↓,
ROS↑, CS internalization in DCs caused mitochondrial stress and led to the production of reactive oxygen species (ROS)
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AD, |
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*TMAO↑, The gut microbiota’s role in metabolizing phytoestrogens suggests that these compounds can modulate the microbial community structure, potentially affecting the production of TMAO from dietary choline and carnitine [5].
*ROS↑, TMAO has the ability to induce oxidative stress in cells by promoting the production of reactive oxygen species (ROS).
*NADPH↑, TMAO has been shown to increase the activity of NADPH oxidase [30], an enzyme that generates ROS as part of its normal function.
*Ca+2↑, TMAO enters platelets and facilitates the release of calcium ions (Ca2+) from intracellular stores.
*AntiAg↓, Calcium serves as a critical secondary messenger in platelet activation, and its elevated levels promote platelet aggregation and thrombus formation
*cognitive↓, TMAO has been linked to cognitive decline and neurodegenerative disorders, including Alzheimer’s disease (AD). Through an integrated analysis of genetic, epigenetic, pathological, and biochemical data, Xu et al. identified a correlation between gut m
*TJ↓, However, excessive TMAO concentrations disrupt BBB integrity by inhibiting tight junction proteins, including claudin-5 and zonula occludens-1
*CLDN1↓,
*ZO-1↓,
*Inflam↑, TMAO also triggers neuroinflammation by activating the NLRP3 inflammasome,
*NLRP3↑,
*ER Stress↑, TMAO enhances the ER stress response by activating the PERK-eIF2α pathway, which is known to impair synaptic plasticity and neuronal function, processes strongly implicated in AD progression
*cognitive↓, TMAO has been identified as the most predictive biomarker for memory impairment and cognitive decline among 56 microbiota-derived metabolic markers
*Dose↝, use of cooking methods such as boiling or stewing instead of grilling, which can produce higher amounts of TMAO
*eff↑, Studies suggest that Lactobacillus plantarum ZDY04 could help reduce TMAO concentrations and prevent TMAO-induced atherosclerosis in animal models
*other↝, Currently, no medications specifically designed to reduce blood TMAO levels exist
*other↝, a review published in 2025 has highlighted the potential role of statins in lowering TMAO levels independently of their cholesterol-lowering effects
*other↝, scientific evidence suggests that statins selectively inhibit the growth of pathogenic bacteria, such as Clostridium and Ruminococcus, while promoting beneficial species, such as Bifidobacterium and Lactobacillus
TumCG↓, inhibition of tumor cell growth via induction of apoptosis, cell-cycle arrest, anti-metastasis and anti-angiogenesis are major promising chemo-preventive actions of cucurbitacins.
Apoptosis↑,
TumCCA↑,
TumMeta↓,
angioG↓,
chemoPv↑,
BioAv↓, CuB has been studied to be ~10% with plasma concentration ranging from 4.85 to 7.81 μg/L after 30 mins of oral dosing.
Half-Life↝, Studies have shown that they reach highest plasma concentration within 1.75 h and an elimination half-life of ~2.5 h.
cycD1/CCND1↓, decreased Cyclin D1 and Cyclin E1 levels.
cycE/CCNE↓,
Casp3↑, CRC cell lines underwent in vitro cell death when exposed to CuB, which was accompanied by caspase-3 and cleaved PARP
cl‑PARP↑,
JNK↑, (TNBC), cucurbitacin E strongly boosted JNK activation while considerably decreasing AKT and ERK activation in MDA-MB-468 cells.
Akt↓,
ERK↓,
survivin↓, also significantly decreased expression of Cyclin D1, Survivin, XIAP, Bcl2 and Mcl-1
XIAP↓,
Bcl-2↓,
Mcl-1↓,
ROS↑, In the pancreatic cancer cell line Capan-1, CuD induced cell-cycle arrest and death via the ROS/p38 pathway [43
NRF2↓, Recent studies have shown that CuIIb and cucurbitacin B induced apoptosis in cervical cancer cell lines by Nrf2 inhibition,
FAK↓, It successfully inhibited angiogenesis by targeting the FAK/MMP-9 signaling axis
MMP9↓,
VEGF↓, suppressed angiogenesis by downregulating the expression of HIF-1 targets, VEGF, VEGFR2 phosphorylation and erythropoietin
VEGFR2↓,
*NF-kB↓, Dietary cucurbitacin E has been shown to reduce inflammation and immunosuppression by downregulating the NF-κB signaling pathway
TLR4↝, Cucurbitacin B was observed to directly bind to toll-like receptor 4 (TLR4) and activate NLRP3 inflammasome, which further ultimately executed pyroptosis in A549 cells.
NLRP3↑,
Pyro↑,
GSH↓, It was observed that treatment with CuI and doxorubicin decreased glutathione (GSH) levels, enhancing cytotoxicity in tumors.
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AD, |
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*Inflam↓, results showed that CuB exhibits potent anti-inflammatory, antioxidant, antiviral, hypoglycemic, hepatoprotective, neuroprotective, and anti-cancer activities
*antiOx↑,
*hepatoP↑,
*neuroP↑,
*AntiCan↑,
*toxicity↝, Studies of its toxicity and pharmacokinetic properties showed that CuB has non-specific toxicity and low bioavailability.
*BioAv↓,
*HO-1↑, CuB can exert its anti-inflammatory effect via the induction of heme oxygenase-1 (HO-1) by the activation Nrf2 [25].
*NRF2↑,
*NLRP3↑, CuB could act as an anti-inflammatory agent to inhibit gouty arthritis in mice [28]. The mechanism of action was mainly attributed to inhibition of the formation and activation of the NOD-like receptor thermal protein domain associated protein 3 (NLR
*SOD↑, Its antioxidant activity may be indirectly realized by increasing the activities of the antioxidant enzymes total SOD and SOD-1, and thereby eliminating excessive ROS and other free radicals in cells
*SOD1↑,
*ROS↓,
*AntiAge↑, this study also confirmed that CuB could exert anti-aging effects by regulating autophagy, ROS, and aging-related genes, which suggested that CuB might be a promising anti-aging drug
*ARE↑, activating the Nrf2/ARE signaling pathway and inhibiting the STAT/NF-κB signaling pathway, and thereby exerting a protective effect on cortical neurons
*STAT↓,
*NF-kB↓,
*neuroG↑, CuB (0.1 mg/kg) could also promote neurogenesis in APP/PS1 mice and alleviate memory deficits associated with enhanced neurogenesis in mice.
*memory↑,
ROS↑, Figure 2
NLRP3↑,
CIP2A↓,
Akt↓,
STAT3↑,
VEGFR2↓,
DNMTs↓, tudies have shown that in H1299 human lung cancer cells CuB (6, 60, 600, and 860 nM) can inhibit DNA methyltransferases (DNMTs)
MAPK↓,
YAP/TEAD↓,
PI3K↓,
Wnt↓,
NOTCH↓,
TumCCA↑,
TumCG↓, Inhibit cell growth and proliferation
TumCP↓,
FAK↑, CuB inhibited the migration, invasion, and adhesion of KKU-452 CCA cells in a dose-dependent manner by suppressing the activation of FAK and down-regulating MMP-9,
MMP9↓,
TumAuto↑, CuB ccould induce autophagy in BEL-7402 hepatocellular carcinoma cells by affecting autophagy-related proteins, such as up-regulating the expression of light chain 3 (LC3)-II
toxicity↝, Most experiments have demonstrated that CuB is moderately cytotoxic, both to human cancer cells and to normal cells
BioAv↓, When Wistar rats were given CuB orally at a dose of 8 mg/kg, the absorption degree was low and the absorption speed was slowest, which was specifically reflected in the fact that the time to peak concentration was longest (180 min, Tmax = 3 h). T
Half-Life↝, When CuB was administered intravenously at 0.1 mg/kg and orally at 1 mg/kg, the clearance rates of CuB in Wistar rats were similar, with a half-life (t1/2) of 5.08 ± 2.87 h and 5.09 ± 2.20 h, respectively [139].
BioAv↑, CuB-loaded mixed micelles with collagen peptides as a carrier, which improved the solubility of CuB and enhanced the absorption of orally administered CuB, and its relative bioavailability increased by a factor of 3.43
selectivity∅, Although CuB displays potent activity against tumor cells, its non-selective toxicity has limited its clinical applications.
*Inflam↓, anti-inflammatory and antioxidant effects of hydrogen gas are attributed to its ability to target reactive oxygen species (ROS) and inhibit NLRP3 inflammasome activation in macrophages
*antiOx↑,
*ROS↓,
*NLRP3↑,
*NF-kB↓, inhibiting the activation of the transcription factor NF-κB
*SOD↑, hydrogen gas regulates the expression of antioxidant enzymes like superoxide dismutase (SOD) and catalase, providing protection against oxidative stress-induced damage
*Catalase↑,
*AntiAg↑, Additionally, Qian et al. found that hydrogen-rich saline may inhibit collagen-induced platelet aggregation in healthy volunteers’ blood samples.
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*ROS↓, inhalation of 2% molecular hydrogen results in the selective scavenging of hydroxyl free radical (·OH) and peroxynitrite anion (ONOO-), significantly improving oxidative stress injury caused by cerebral ischemia/reperfusion (I/R)
eff↝, Molecular hydrogen can exert biological effects on almost all organs, including the brain, heart, lung, liver, and pancreas.
*Inflam↓, including roles in the regulation of oxidative stress and anti-inflammatory and anti-apoptotic effects
*NRF2↑, By stimulating nuclear factor erythroid 2-related factor 2 (Nrf2), which regulates the basal and induces expression of many antioxidant enzymes
*HO-1↑, hydrogen can increase the expression of heme oxygenase-1 (HO-1)
*SOD↑, increases the activity of the antioxidant enzymes SOD, CAT, and myeloperoxidase (MPO)
*Catalase↑,
*MPO↑,
*ASK1↓, Molecular hydrogen can block the apoptosis signal-regulating kinase 1 (ASK1) signaling pathway
*NADPH↓, thereby inhibiting nicotinamide adenine dinucleotide phosphate (NADPH) oxidase activity and decreasing free radical production
*Sepsis↓, Emerging evidence suggests that hydrogen can prevent sepsis, providing a novel treatment strategy for sepsis-induced ALI.
*HMGB1↓, Hydrogen attenuates tissue injury and dysfunction by inhibiting HMGB-1.
ROS↑, it has been shown that hydrogen pretreatment enhances ROS and the expression of pyroptosis-related proteins, stimulates NLRP3 inflammasome/gasdermin D (GSDMD) activation, and inhibits endometrial cancer
NLRP3↑,
GSDMD↑,
chemoP↑, Hydrogen can alleviate the side effects of conventional anti-cancer therapies, such as chemotherapy and radiotherapy, and improve quality of life
eff↑, It significantly improves the physical status of patients, reduces fatigue, insomnia, anorexia, and pain, and decreases elevated tumor markers.
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ESCC, |
KYSE-30 |
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Pyro↑, PL significantly suppressed malignant behavior by promoting pyroptosis of ESCC cells by inhibiting proliferation, migration, invasion, and colony formation of KYSE-30 cells
TumCP↓,
TumCMig↓,
TumCI↓,
ASC↑, up-regulating expressions of ASC, Cleaved-caspase-1, NLRP3, and GSDMD, while inducing the generation of ROS.
cl‑Casp1↑,
NLRP3↑,
GSDMD↑,
ROS↑,
NRF2↓, PL inhibited the malignant behavior of ESCC cells in vitro and tumorigenesis of ESCC in vivo by inhibiting NRF2 and promoting ROS-TXNIP-NLRP3-mediated pyroptosis.
TXNIP↑,
Showing Research Papers: 1 to 8 of 8
* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 8
Pathway results for Effect on Cancer / Diseased Cells:
Redox & Oxidative Stress ⓘ
GSH↓, 1, NRF2↓, 2, ROS↑, 5,
Mitochondria & Bioenergetics ⓘ
XIAP↓, 1,
Cell Death ⓘ
Akt↓, 2, Apoptosis↑, 1, Bcl-2↓, 1, Casp1↓, 1, cl‑Casp1↑, 1, Casp3↑, 1, GSDMD↑, 2, JNK↑, 1, MAPK↓, 1, Mcl-1↓, 1, Pyro↑, 2, survivin↓, 1, YAP/TEAD↓, 1,
Protein Folding & ER Stress ⓘ
CHOP↑, 1, ER Stress↑, 1,
Autophagy & Lysosomes ⓘ
LC3B↑, 1, TumAuto↑, 2,
DNA Damage & Repair ⓘ
DNMTs↓, 1, cl‑PARP↑, 1,
Cell Cycle & Senescence ⓘ
cycD1/CCND1↓, 1, cycE/CCNE↓, 1, TumCCA↑, 2,
Proliferation, Differentiation & Cell State ⓘ
CIP2A↓, 1, ERK↓, 1, NOTCH↓, 1, PI3K↓, 1, STAT1↑, 1, STAT3↑, 1, TumCG↓, 2, Wnt↓, 1,
Migration ⓘ
FAK↓, 1, FAK↑, 1, MMP9↓, 2, TumCI↓, 1, TumCMig↓, 1, TumCP↓, 2, TumMeta↓, 1, TXNIP↑, 1,
Angiogenesis & Vasculature ⓘ
angioG↓, 1, EPR↑, 1, VEGF↓, 1, VEGFR2↓, 2,
Immune & Inflammatory Signaling ⓘ
ASC↑, 1, IL1β↓, 1, Imm↑, 1, TLR4↝, 1,
Cellular Microenvironment ⓘ
cGAS–STING↑, 1,
Protein Aggregation ⓘ
NLRP3↑, 6,
Drug Metabolism & Resistance ⓘ
BioAv↓, 2, BioAv↑, 1, DDS↑, 1, eff↑, 1, eff↝, 1, Half-Life↝, 2, selectivity∅, 1,
Functional Outcomes ⓘ
chemoP↑, 1, chemoPv↑, 1, toxicity↝, 1,
Total Targets: 62
Pathway results for Effect on Normal Cells:
NA, unassigned ⓘ
TMAO↑, 1,
Redox & Oxidative Stress ⓘ
antiOx↑, 2, ARE↑, 1, Catalase↑, 2, HO-1↑, 2, MPO↑, 1, NRF2↑, 2, ROS↓, 3, ROS↑, 1, SOD↑, 3, SOD1↑, 1,
Core Metabolism/Glycolysis ⓘ
NADPH↓, 1, NADPH↑, 1,
Cell Death ⓘ
ASK1↓, 1,
Transcription & Epigenetics ⓘ
other↝, 3,
Protein Folding & ER Stress ⓘ
ER Stress↑, 1,
Proliferation, Differentiation & Cell State ⓘ
neuroG↑, 1, STAT↓, 1,
Migration ⓘ
AntiAg↓, 1, AntiAg↑, 1, Ca+2↑, 1, Cartilage↑, 1, CLDN1↓, 1, TGF-β1↓, 1, TJ↓, 1, ZO-1↓, 1,
Immune & Inflammatory Signaling ⓘ
DCells↑, 1, HMGB1↓, 1, IL10↓, 1, Inflam↓, 3, Inflam↑, 1, NF-kB↓, 3, TNF-α↓, 1,
Protein Aggregation ⓘ
NLRP3↑, 3,
Drug Metabolism & Resistance ⓘ
BioAv↓, 1, Dose↝, 1, eff↑, 1,
Functional Outcomes ⓘ
AntiAge↑, 1, AntiCan↑, 1, cognitive↓, 2, hepatoP↑, 1, memory↑, 1, neuroP↑, 1, toxicity↝, 1, Wound Healing↑, 1,
Infection & Microbiome ⓘ
Sepsis↓, 1,
Total Targets: 46
Scientific Paper Hit Count for: NLRP3, NOD-like receptor pyrin domain-containing protein 3
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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