Casp1 Cancer Research Results

Casp1, Caspase-1: Click to Expand ⟱

Source:

Type:

Also known as ICE (Interleukin-1 beta Convertase).
Caspases are a cysteine protease that speed up a chemical reaction via pointing their target substrates following an aspartic acid residue.1 They are grouped into apoptotic (caspase-2, 3, 6, 7, 8, 9 and 10) and inflammatory (caspase-1, 4, 5, 11 and 12) mediated caspases.
Caspase-1 may have both tumorigenic or antitumorigenic effects on cancer development and progression, but it depends on the type of inflammasome, methodology, and cancer.
Caspase-1:
Role: Involved in inflammation and pyroptosis.
Cancers: Elevated in certain cancers, including colorectal cancer and pancreatic cancer.
Prognosis: High levels may be associated with a more aggressive tumor phenotype.

Scientific Papers found: Click to Expand⟱

5146-

AgNPs,

Silver Nanoparticle-Induced Autophagic-Lysosomal Disruption and NLRP3-Inflammasome Activation in HepG2 Cells Is Size-Dependent

in-vitro,

Liver,

HepG2

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↓,

2693-

BBR,

Antitumor Effects of Berberine on Gliomas via Inactivation of Caspase-1-Mediated IL-1β and IL-18 Release

in-vitro,

GBM,

U251

in-vitro,

GBM,

U87MG

Casp1↓, berberine significantly inhibits inflammatory cytokine Caspase-1 activation via ERK1/2 signaling and subsequent production of IL-1β and IL-18 by glioma cells.
ERK↓, berberine induces senescence of human glioma cells by downregulating the extracellular kinase/mitogen-activated protein kinase (ERK/MAPK) signaling pathway
IL1β↓, Berberine Exhibit Inhibitory Effects on Caspase-1, IL-18, and IL-1β Proteins
IL18↓,
EMT↑, berberine can reverse the process of epithelial-mesenchymal transition. aken together, these results suggest that berberine can inhibit the process of EMT

2692-

BBR,

Berberine affects osteosarcoma via downregulating the caspase-1/IL-1β signaling axis

in-vitro,

OS,

MG63

in-vitro,

OS,

SaOS2

in-vivo,

NA,

mice

Casp1↓, administration of berberine is capable of reducing the expression of caspase-1 and IL-1β in osteosarcoma cells and inhibiting the growth of tumor cells.
IL1β↓,
TumCG↓,
Dose↝, concentration of berberine at 80 µM could inhibit the cell viability to the greatest extent; and the viable cells at 48 h decreased more obviously than 24 h after treatment with 80 µM berberine.
Apoptosis↑, Berberine induces apoptosis of Saos-2 and MG-63 osteosarcoma cells
Inflam↓, these observations demonstrate that berberine could probably relieve the inflammation in tumor microenvironment and then results in apoptosis of osteosarcoma cells.

1092-

BBR,

Berberine as a Potential Anticancer Agent: A Comprehensive Review

Review,

NA,

0.2-0.5uM

U87 and U251 human glioblastoma cell lines in BALB/c nude mice (IC50 of 42 and 32 μmol/L, respectively).

Apoptosis↑,
TumCCA↑,
TumAuto↑,
TumCI↓,
IL1↓, IL-1α, IL-1β
IL6↓,
TNF-α↓,
LDH↓, BBR also increases the release of Lactic Acid Dehydrogenase (LDH) in the MDA epithelial human breast cancer cell line (MDA-cells)
P2X7↓,
proCasp1↓,
Casp1↓,
ASC↓,

5483-

BM,

The Role of Bacopa monnieri in Alzheimer’s Disease: Mechanisms and Potential Clinical Use—A Review

Review,

AD,

*cognitive↑, Bacopa monnieri, also known as brahmi, which has gained particular popularity for its cognitive-function-enhancing properties and neuroprotective effects.
*neuroP↑,
*PI3K↑, figure 3
*Akt↑,
*GSK‐3β↓,
*tau↓,
*ROS↓,
*MMP3↓,
*Casp1↓,
*Casp3↓,
*NF-kB↓,
*TNF-α↓,
*IL6↓,

5875-

CA,

Carnosic acid prevents dextran sulfate sodium-induced acute colitis associated with the regulation of the Keap1/Nrf2 pathway

in-vivo,

IBD,

mice

*antiOx↑, Carnosic acid (CA) has been reported to possess antioxidative properties
*Weight↑, CA significantly prevented the loss of body weight and shortening of colon length in acute colitis induced by dextran sodium sulfate (DSS).
*p65↓, CA decreased the activation of p65 and c-Jun signalling.
*cJun↓,
*NLRP3↓, CA inhibited DSS-induced NLRP3 inflammasome activation by reducing caspase 1 activity.
*Casp1↓,
*NRF2↑, CA increased the level of Nrf2 and prevented the degradation of Nrf2 via ubiquitination by blocking the interaction between Cullin3 and Keap1,
*GSH↑, Finally, GSH levels and SOD activity were increased after CA treatment, while MDA and iNOS levels were significantly reduced.
*SOD↑,
*MDA↓,
*iNOS↓,
other↝, Moreover, many compounds from natural products, such as ellagic acid, gallic acid and quercetin, have been shown to prevent IBD through their antioxidative properties

3225-

EGCG,

Epigallocatechin‐3‐Gallate Ameliorates Diabetic Kidney Disease by Inhibiting the TXNIP/NLRP3/IL‐1β Signaling Pathway

in-vitro,

Nor,

Human podocytes

in-vivo,

Nor,

mice

*RenoP↑, EGCG improved kidney function, reduced albuminuria and body weight, and alleviated renal pathological damage.
*NLRP3↓, EGCG treatment reduced the expression of the NLRP3 inflammasome and its associated proteins, including TXNIP, ASC, caspase‐1, and IL‐1β, as well as the levels of ROS and inflammatory factors such as TNF‐α, IL‐6, and IL‐18.
*TXNIP↓,
*ASC↓,
*Casp1↓,
*IL1β↓,
*ROS↓,
*TNF-α↓,
*IL6↓,
*IL18↓,

3224-

EGCG,

Epigallocatechin-3-Gallate Prevents Acute Gout by Suppressing NLRP3 Inflammasome Activation and Mitochondrial DNA Synthesis

in-vitro,

Nor,

mice

*Casp1↓, EGCG blocked MSU crystal-induced production of caspase-1(p10) and interleukin-1β in primary mouse macrophages, indicating its suppressive effect on the NLRP3 inflammasome.
*NLRP3↓,
*Inflam↓, contributing to the prevention of gouty inflammation

2921-

LT,

Luteolin as a potential hepatoprotective drug: Molecular mechanisms and treatment strategies

Review,

Nor,

*hepatoP↑, Due to its excellent liver protective effect, luteolin is an attractive molecule for the development of highly promising liver protective drugs.
*AMPK↑, fig2
*SIRT1↑,
*ROS↓,
STAT3↓,
TNF-α↓,
NF-kB↓,
*IL2↓,
*IFN-γ↓,
*GSH↑,
*SREBP1↓,
*ZO-1↑,
*TLR4↓,
BAX↑, anti cancer
Bcl-2↓,
XIAP↓,
Fas↑,
Casp8↑,
Beclin-1↑,
*TXNIP↓, luteolin inhibited TXNIP, caspase-1, interleukin-1β (IL-1β) and IL-18 to prevent the activation of NLRP3 inflammasome, thereby alleviating liver injury.
*Casp1↓,
*IL1β↓,
*IL18↓,
*NLRP3↓,
*MDA↓, inhibiting oxidative stress and regulating the level of malondialdehyde (MDA), superoxide dismutase (SOD) and glutathione (GSH)
*SOD↑,
*NRF2↑, luteolin promoted the activation of the Nrf2/ antioxidant response element (ARE) pathway and NF-κB cell apoptosis pathway, thereby reversing the decrease in Nrf2 levels(lead induced liver injury)
*ER Stress↓, down regulate the formation of nitrotyrosine (NT) and endoplasmic reticulum (ER) stress induced by acetaminophen, and alleviate liver injury
*ALAT↓, ↓ALT, AST, MDA, iNOS, NLRP3 ↑GSH, SOD, Nrf2
*AST↓,
*iNOS↓,
*IL6↓, ↓TXNIP, NLRP3, TNF-α, IL-6 ↑HO-1, NQO1
*HO-1↑,
*NQO1↑,
*PPARα↑, ↓TNF-α, IL-6 IL-1β, Bax ↑PPARα
*ATF4↓, ↓ALT, AST, TNF-α, IL-6, MDA, ATF-4, CHOP ↑GSH, SOD
*CHOP↓,
*Inflam↓, Luteolin ameliorates MAFLD through anti-inflammatory and antioxidant effects
*antiOx↑,
*GutMicro↑, luteolin could significantly enrich more than 10% of intestinal bacterial species, thereby increasing the abundance of ZO-1, down regulating intestinal permeability and plasma lipopolysaccharide

2919-

LT,

Luteolin as a potential therapeutic candidate for lung cancer: Emerging preclinical evidence

Review,

Var,

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

3471-

MF,

The prevention effect of pulsed electromagnetic fields treatment on senile osteoporosis in vivo via improving the inflammatory bone microenvironment

in-vivo,

Nor,

PEMF with 40 min/day, five days per week

24 Sprague Dawley (SD) rats

*BMD↑, PEMF increased the bone mineral density of the proximal femur and L5 vertebral body and improved parameters of the proximal tibia and L4 vertebral body.
*NLRP3↓, PEMF also dramatically inhibited NLRP3-mediated low-grade inflammation in the bone marrow,
*proCasp1↓, PEMF inhibited the levels of NLRP3, proCaspase1, cleaved Caspase1, IL-1β, and GSDMD-N.
*cl‑Casp1↓,
*IL1β↓,
*GSDMD↓,

3472-

MF,

Pulsed electromagnetic field alleviates synovitis and inhibits the NLRP3/Caspase-1/GSDMD signaling pathway in osteoarthritis rats

in-vivo,

ostP,

3.82 mT, 8 Hz, 40 min/day, 5 days a week, for 12 weeks.

three-month-old Sprague-Dawley (SD)

*Inflam↓, Pulsed electromagnetic field (PEMF) can improve the symptoms of OA and potentially acts as an anti-inflammatory
*NLRP3↓, the over-expression of NLRP3, Caspase-1, and GSDMD in the cartilage of the OA rats decreased after PEMF treatment.
*Casp1↓,
*GSDMD?,

2972-

PL,

Piperlongumine Is an NLRP3 Inhibitor With Anti-inflammatory Activity

in-vitro,

AML,

THP1

NLRP3↓, PL is a natural inhibitor of Nod-like receptor family pyrin domain-containing protein-3 (NLRP3) inflammasome,
IL1β↓, We further observed that PL inhibited IL-1β secretion, LDH release, and caspase-1 cleavage when macrophages were treated with other NLRP3 agonists, including ATP and MSU
LDH↓,
cl‑Casp1↓,
Inflam↓, Piperlongumine Suppresses NLRP3-Dependent Inflammation in vivo

3003-

RosA,

Comprehensive Insights into Biological Roles of Rosmarinic Acid: Implications in Diabetes, Cancer and Neurodegenerative Diseases

Review,

Var,

Review,

AD,

Review,

Park,

*Inflam↓, anti-inflammatory and antioxidant properties and its roles in various life-threatening conditions, such as cancer, neurodegeneration, diabetes,
*antiOx↑,
*neuroP↑,
*IL6↓, diabetic rat model treated with RA, there is an anti-inflammatory activity reported. This activity is achieved through the inhibition of the expression of various proinflammatory factors, including in IL-6, (IL-1β), tumour
*IL1β↓,
*NF-kB↓, inhibiting NF-κB activity and reducing the production of prostaglandin E2 (PGE2), nitric oxide (NO), and cyclooxygenase-2 (COX-2) in RAW 264.7 cells.
*PGE2↓,
*COX2↓,
*MMP↑, RA inhibits cytotoxicity in tumour patients by maintaining the mitochondrial membrane potential
*memory↑, amyloid β(25–35)-induced AD in rats was treated with RA, which mitigated the impairment of learning and memory disturbance by reducing oxidative stress
*ROS↓,
*Aβ↓, daily consumption of RA diminished the effect of neurotoxicity of Aβ25–35 in mice
*HMGB1↓, SH-SY5Y in vitro and ischaemic diabetic stroke in vivo, and the studies revealed that a 50 mg/kg dose of RA decreased HMGB1 expression
TumCG↓, Rosemary and its extracts have been shown to exhibit potential in inhibiting the growth of cancer cells and the development of tumours in various cancer types, including colon, breast, liver, and stomach cancer
MARK4↓, Another study reported the inhibition of Microtubule affinity regulating kinase 4 (MARK4) by RA
Zeb1↓, Fig 4 BC:
MDM2↓,
BNIP3↑,
ASC↑, Skin Cancer
NLRP3↓,
PI3K↓,
Akt↓,
Casp1↓,
E-cadherin↑, Colon Cancer
STAT3↓,
TLR4↓,
MMP↓,
ICAM-1↓,
AMPK↓,
IL6↑, PC and GC
MMP2↓,
Warburg↓,
Bcl-xL↓, CRC: Apoptosis induction caspases ↑, Bcl-XL ↓, BCL-2 ↓, Induces cell cycle arrest, Inhibition of EMT and invasion, Reduced metastasis
Bcl-2↓,
TumCCA↑,
EMT↓,
TumMeta↓,
mTOR↓, Inhibits mTOR/S6K1 pathway to induce apoptosis in cervical cancer
HSP27↓, Glioma ↓ expression of HSP27 ↑ caspase-3
Casp3↑,
GlucoseCon↓, GC: Inhibited the signs of the Warburg effect, such as high glucose consumption/anaerobic glycolysis, lactate production/cell acidosis, by inhibiting the IL-6/STAT3 pathway
lactateProd↓,
VEGF↓, ↓ angiogenic factors (VEGF) and phosphorylation of p65
p‑p65↓,
GIT1↓, PC: Increased degradation of Gli1
FOXM1↓, inhibiting FOXM1
cycD1/CCND1↓, RA treatment in CRC cells inhibited proliferation-induced cell cycle arrest of the G0/G1 phase by reducing the cyclin D1 and CDK4 levels,
CDK4↓,
MMP9↓, CRC cells, and it led to a decrease in the expressions of matrix metalloproteinase (MMP)-2 and MMP-9.
HDAC2↓, PCa cells through the inhibition of HDAC2

3186-

SFN,

A pharmacological inhibitor of NLRP3 inflammasome prevents non-alcoholic fatty liver disease in a mouse model induced by high fat diet

in-vivo,

Nor,

30 mg/kg/day

mice

*NLRP3↓, suppression of NLRP3 inflammasome activation in the liver by SFN as evidenced by decrease in mRNA levels of ASC and caspase-1, caspase-1 enzyme activity, and IL-1β levels.
*ASC↓,
*Casp1↓,
*IL1β↓,
*ALAT↓, SFN treatment resulted in a reduction of the serum levels of ALT and AST increased by HFD
*AST↓,
*AMPK↑, Sulforaphane induces activation of the AMPK-autophagy axis in mouse primary hepatocytes
*mTOR↓, SFN reduced the phosphorylation of mTOR(Ser2448) in primary mouse hepatocytes (Fig. 4D), suggesting that SFN inhibited mTOR activation
*P70S6K↓, SFN suppression of mTOR activation was confirmed by a decrease in p70S6K1 phosphorylation, which is a downstream substrate of mTOR

2354-

SK,

PKM2-dependent glycolysis promotes NLRP3 and AIM2 inflammasome activation

in-vivo,

Sepsis,

mice

PKM2↓, Shikonin is a potent PKM2 inhibitor in cancer cells and macrophages
*PKM2↓,
*IL1β↓, Shikonin dose-dependently inhibited IL-1β, IL-18 and HMGB1 release in activated BMDMs following treatment with NLRP3 inflammasome activator (for example, ATP) or AIM2 inflammasome activator
*IL18↓,
*HMGB1↓,
*Casp1↓, shikonin significantly inhibited caspase-1 activation triggered by stimulation with ATP
*NLRP3↓, pharmacologic inhibition of PKM2 by shikonin selectively suppresses NLRP3 and AIM2 inflammasome activation.
*AIM2↓,
*p‑eIF2α↓, Shikonin inhibited EIF2AK2 phosphorylation (Fig. 6a) and caspase-1 activity (Fig. 6b) in PMs obtained from mice subjected to lethal endotoxemia or polymicrobial sepsis.
*Sepsis↓,

3420-

TQ,

Thymoquinone alleviates the accumulation of ROS and pyroptosis and promotes perforator skin flap survival through SIRT1/NF-κB pathway

in-vitro,

Nor,

HUVECs

in-vitro,

NA,

rat

*NF-kB↓, TQ improves perforator flap survival by inhibiting the NF-κB/NLRP3 pathway and promoting angiogenesis.
*NLRP3↓,
*angioG↑,
*MMP9↑, TQ treatment increased the levels of Cadherin-5, MMP9, and VEGF
*VEGF↑,
*OS↑, TQ enhances the survival rate and angiogenesis of multi-regional perforator flaps.
*Pyro?, TQ inhibits pyroptosis after ischemia-reperfusion injury in rat perforator flaps
*ROS↓, TQ ameliorates oxidative stress and apoptosis following ischemia-reperfusion injury in rat perforator flaps
*Apoptosis↓,
*SIRT1↑, Western blot analysis revealed that SIRT1 protein expression increased after TQ treatment,
*SOD1↑, TQ treatment increased the protein expression levels of SOD1, HO1, and eNOS in rat perforator flap tissues, t
*HO-1↑,
*eNOS↑,
*ASC?, In our current experiments, we found that TQ reduced the expression of NLRP3, GSDMD-N, Caspase-1, IL-1β, IL-18, and ASC proteins both in vivo and in vitro.
*Casp1↓,
*IL1β↓,
*IL18↓,

3418-

TQ,

Thymoquinone suppresses metastasis of melanoma cells by inhibition of NLRP3 inflammasome

in-vitro,

Melanoma,

A375

in-vivo,

NA,

B16F10) melanoma cell line

TumMeta↓, Thymoquinone causes inhibition of metastasis in vivo
TumCMig↓, Thymoquinone causes inhibition of migration by activation of NLRP3 inflammasome.
NLRP3↓,
Casp1↓, Inactivation of caspase-1 by thymoquinone resulted in inhibition of IL-1β and IL-18.
IL1β↓,
IL18↓,
ROS↓, Furthermore, inhibition of reactive oxygen species (ROS) by thymoquinone resulted in partial inactivation of NLRP3 inflammasome.
NF-kB↓, as well as inhibition of NF-κB, and hence suppressing growth and migration of melanoma cells.

2277-

VitK2,

Vitamin K2 suppresses rotenone-induced microglial activation in vitro

in-vitro,

Nor,

BV2

MK-4 (0.5–20 μmol/L

NA,

AD,

NA,

Park,

*p38↓, MK-4 (5–20 μmol/L) significantly inhibited rotenone-induced p38 activation, ROS production, and caspase-1 activation in BV2 cells
*ROS↓,
*Casp1↓,
*MMP↑, MK-4 (5–20 μmol/L) also restored the mitochondrial membrane potential that had been damaged by rotenone
*NF-kB↓, inhibiting NF-κB activation
*IL1β↓, MK-4 suppresses rotenone-induced activation of NF-κB and the production of inflammatory factors, including TNF-α, IL-1β, iNOS and COX-2
*iNOS↓, fig1
*COX2↓, fig1
*TNF-α↓, fig1

Showing Research Papers: 1 to 19 of 19

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 19

Pathway results for Effect on Cancer / Diseased Cells:

Functional Outcomes ⓘ

cachexia↓, 1, chemoP↑, 1,
Total Targets: 143

Pathway results for Effect on Normal Cells:

Redox & Oxidative Stress ⓘ

antiOx↑, 3, Catalase↑, 1, GPx↑, 1, GSH↑, 3, GSTs↑, 1, HO-1↑, 2, lipid-P↓, 1, MDA↓, 2, NQO1↑, 1, NRF2↑, 2, ROS↓, 6, SOD↑, 3, SOD1↑, 1,

Mitochondria & Bioenergetics ⓘ

MMP↑, 2,

Core Metabolism/Glycolysis ⓘ

ALAT↓, 2, AMPK↑, 2, PKM2↓, 1, PPARα↑, 1, SIRT1↑, 2, SREBP1↓, 1,

Cell Death ⓘ

Akt↑, 1, Apoptosis↓, 1, Casp1↓, 10, cl‑Casp1↓, 1, proCasp1↓, 1, Casp3↓, 2, GSDMD?, 1, GSDMD↓, 1, iNOS↓, 3, p38↓, 1, Pyro?, 1,

Transcription & Epigenetics ⓘ

cJun↓, 1,

Protein Folding & ER Stress ⓘ

CHOP↓, 1, p‑eIF2α↓, 1, ER Stress↓, 1,

Proliferation, Differentiation & Cell State ⓘ

GSK‐3β↓, 1, mTOR↓, 1, P70S6K↓, 1, PI3K↑, 1,

Migration ⓘ

MMP3↓, 1, MMP9↑, 1, TXNIP↓, 2, ZO-1↑, 1,

Angiogenesis & Vasculature ⓘ

angioG↑, 1, ATF4↓, 1, eNOS↑, 1, VEGF↑, 1,

Immune & Inflammatory Signaling ⓘ

AIM2↓, 1, ASC?, 1, ASC↓, 2, COX2↓, 2, HMGB1↓, 2, IFN-γ↓, 1, IL10↑, 1, IL18↓, 4, IL1β↓, 9, IL2↓, 1, IL6↓, 4, Inflam↓, 4, NF-kB↓, 4, p65↓, 1, PGE2↓, 1, TLR4↓, 1, TNF-α↓, 4,

Synaptic & Neurotransmission ⓘ

tau↓, 1,

Protein Aggregation ⓘ

Aβ↓, 1, NLRP3↓, 9,

Drug Metabolism & Resistance ⓘ

eff↑, 1, Half-Life↝, 1,

Clinical Biomarkers ⓘ

ALAT↓, 2, AST↓, 2, BMD↑, 1, GutMicro↑, 1, IL6↓, 4,

Functional Outcomes ⓘ

cognitive↑, 1, hepatoP↑, 1, memory↑, 1, neuroP↑, 2, OS↑, 1, RenoP↑, 1, Weight↑, 1,

Infection & Microbiome ⓘ

Sepsis↓, 1,
Total Targets: 82

Scientific Paper Hit Count for: Casp1, Caspase-1

3 Berberine
2 EGCG (Epigallocatechin Gallate)
2 Luteolin
2 Magnetic Fields
2 Thymoquinone
1 Silver-NanoParticles
1 Bacopa monnieri
1 Carnosic acid
1 Piperlongumine
1 Rosmarinic acid
1 Sulforaphane (mainly Broccoli)
1 Shikonin
1 Vitamin K2

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#:41  State#:%  Dir#:1
  wNotes=on  sortOrder:rid,rpid

Casp1 Cancer Research Results

Pathway results for Effect on Cancer / Diseased Cells:

Redox & Oxidative Stress ⓘ

Mitochondria & Bioenergetics ⓘ

Core Metabolism/Glycolysis ⓘ

Cell Death ⓘ

Transcription & Epigenetics ⓘ

Protein Folding & ER Stress ⓘ

Autophagy & Lysosomes ⓘ

DNA Damage & Repair ⓘ

Cell Cycle & Senescence ⓘ

Proliferation, Differentiation & Cell State ⓘ

Migration ⓘ

Angiogenesis & Vasculature ⓘ

Immune & Inflammatory Signaling ⓘ

Protein Aggregation ⓘ

Hormonal & Nuclear Receptors ⓘ

Drug Metabolism & Resistance ⓘ

Clinical Biomarkers ⓘ

Functional Outcomes ⓘ

Pathway results for Effect on Normal Cells:

Redox & Oxidative Stress ⓘ

Mitochondria & Bioenergetics ⓘ

Core Metabolism/Glycolysis ⓘ

Cell Death ⓘ

Transcription & Epigenetics ⓘ

Protein Folding & ER Stress ⓘ

Proliferation, Differentiation & Cell State ⓘ

Migration ⓘ

Angiogenesis & Vasculature ⓘ

Immune & Inflammatory Signaling ⓘ

Synaptic & Neurotransmission ⓘ

Protein Aggregation ⓘ

Drug Metabolism & Resistance ⓘ

Clinical Biomarkers ⓘ

Functional Outcomes ⓘ

Infection & Microbiome ⓘ

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