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⟱
5633- BCA,    Mechanisms Behind the Pharmacological Application of Biochanin-A: A review
- Review, Var, NA - Review, AD, NA
*AntiDiabetic↑, Through modulating oxidative stress, SIRT-1 expression, PPAR gamma receptors, and other multiple mechanisms biochanin-A produces anti-diabetic action.
*neuroP↑, Biochanin-A has been shown to have a potential neuroprotective impact by modulating multiple critical neurological pathways.
*toxicity↓, Unlike chemical agents such as chemotherapeutic agents, isoflavones have shown zero toxicity to humans
*CYP19↓, Biochanin-A inhibits CYP19 and negatively affects the synthesis of oestrogen in the body which enhances the anti-oestrogenic property in hormone-influenced cancer such as prostate cancer and breast cancer
p‑Akt↓, Biochanin-A inhibits Akt phosphorylation thereby downregulates mTOR signals and disrupts the cell cycle.
mTOR↓,
TumCCA↑,
P21↑, Biochanin-A cause apoptosis in lung cancer by increasing p21, caspase-3, and Bcl-2 levels. It lowers E-cadherin and blocks metastasis.
Casp3↑,
Bcl-2↑,
Apoptosis↑,
E-cadherin↓,
TumMeta↓,
eff↑, The synergism of biochanin-A with 5-fluorouracil evidenced in Caco-2 and HCT-116 cell lines indicates the modulatory influence of biochanin-A in colon cancer treatment.
GSK‐3β↓, It blocked the “Akt and GSK3β phosphorylation and boosted the degradation of β-catenin” ( Mahmoud et al., 2017).
β-catenin/ZEB1↓,
RadioS↑, Biochanin-A when combined with gamma radiation on HT29 cells, which is resistant to radiation, had revealed a reduction in cell proliferation.
ROS↑, Raised levels of ROS, lipid peroxidation, MMP, caspase-3 have been observed more in the treatment group with significant apoptosis
Casp1↑,
MMP2↓, biochanin-A influenced the tumour invasion capacity by lowering matrix-degrading enzymes (MMP 2 and MMP 9) tested in U87MG cells
MMP9↓,
EGFR↓, Biochanin-A by lowering EGFR, p-ERK (Extracellular signal related kinases), p-AKT (Protein kinase-B), c-myc, and MT-MMP1 (Membrane type matrix metalloproteinase) activation, inhibited cell survival.
ChemoSen↑, Biochanin-A synergistically improved temozolomide anti-cancer ability in GBM
PI3K↓, Cell signalling pathways MAP kinase, PI3 kinase, mTOR, matrix metalloproteases, hypoxia-inducible factor, and VEGF were inhibited by biochanin-A, making it suitable in treating GBM
MMPs↓,
Hif1a↓,
VEGF↓,
*ROS↓, anti-diabetic mechanism of biochanin-A is by decreasing oxidative stress
*Obesity↓, strongly suggest that biochanin-A has therapeutic potential in the treatment of obesity and the prevention of cardiovascular disease
*cardioP↑,
*NRF2↑, Biochanin-A up-regulated the Nrf-2 pathway while suppressing the NF-κB cascade,
*NF-kB↓, By activating the Nrf-2 pathway and inhibiting NF-κB activation, biochanin-A may reduce obesity and its related cardiomyopathy by decreasing oxidative stress and inflammation
*Inflam↓,
*lipid-P↓, cardio-protective effects by controlling lipid peroxidation
*hepatoP↑, biochanin-A influence the elevated hepatic enzyme level, such as AST, ALP, ALT, bilirubin, etc., and found to be a promising molecule in hepatotoxicity models
*AST↓,
*ALP↓,
*Bacteria↓, The results indicate that biochanin-A may be an effective alternate to antibiotics for alleviating SARA in cattles
*neuroP↑, the neuroprotective effects of biochanin-A might be attributed to the activation of the Nrf2 pathway and suppression of the NF-κB pathway
*SOD↑, Biochanin-A reduced oxidative stress in the brain by augmenting SOD (superoxide dismutase) and GSH-Px (glutathione peroxidase) and repressing MDA (malondialdehyde) levels.
*GPx↑,
*AChE↓, Acetylcholinesterase activity was found decreased in a dose-reliant manner amongst biochanin-A treated animals
*BACE↓, Biochanin-A non-competitively inhibited BACE1 with an IC 50 value of 28 μM.
*memory↑, estore learning and memory deficits in ovariectomized (OVX) rats.
*BioAv↓, The bioavailability of biochanin-A is poor.

6318- DRE,    Dandelion root extract affects colorectal cancer proliferation and survival through the activation of multiple death signalling pathways
- vitro+vivo, CRC, HCT116 - NA, Nor, NCM460
TumCD↑, Aqueous DRE induced programmed cell death (PCD) selectively in > 95% of colon cancer cells, irrespective of their p53 status, by 48 hours of treatment.
Apoptosis↑, Furthermore, the induction of apoptosis is dependent on caspase-8 activation
Casp8↑,
selectivity↑, The selectivity of DRE to cancer cells was once again confirmed, as normal NCM460 cells were DRE refractive and did not lose metabolic activity and cell viability when exposed to the same doses
TumCMig↓, Dandelion root extract selectively impairs the migration of colon cancer cells
selectivity↑, the normal NCM460 cells treated with DRE were able to migrate into the scratch wound area
Dose↝, DRE administration to normal Balb/c mice, at a dose of 40 mg/kg/day, for a period of 75 days.
toxicity↓, these results established that systemic oral intake of the DRE was safe and its anti-cancer efficacy should be further investigated.
TumCG↓, was efficacious in halting the growth of colon tumors in xenograft models.
MMP↓, loss of mitochondrial membrane potential, in HT-29 cells, with no difference between the control and DRE treated samples of NCM460
mt-ROS↑, results showed a significant increase in the levels of ROS produced in the DRE-treated mitochondria of HT-29 cells
*ROS↓, DRE treatment of isolated mitochondria from NCM460 cells did not produce any significant amounts of ROS. being able to scavenge reactive oxygen species in mouse macrophage cells, RAW264.7
BID↑, DRE treatment led to the truncation of Bid in HT-29 cells selectively, with no increase in Bid truncation in NCM460 cells
Bcl-2↓, table 2
PARP↓,
NF-kB↑, +1.1 fold
*NF-kB↓, -2.3 fold
Casp1↑, +12.3 fold
*Casp1↓, -2.5 fold
COX2↑, DRE treatment selectively decreased the expression of COX-2 in colon cancer cells in a dose and time dependent manner, showing its potential as an anti-inflammatory extract.
OXPHOS↓, altered oxidative phosphorylation and reduced flux through the electron transport chain
ETC↓,

6363- DRE,    Therapeutic Potential of Dandelion (Taraxacum officinale) Root Extract in Colon Cancer: A Comprehensive Review
- in-vitro, CRC, NA
Apoptosis↑, highlighting its ability to induce apoptosis, inhibitpro-inflammatory pathways like TLR4/NF-κB, and modulate gut microbiota.
*Inflam↓,
TLR4↓,
NF-kB↓,
*GutMicro↑, DRE modulates the gut microbiota composition,increasing the abundance of short-chain fatty acid-producing bacteria such as Lactobacillus and Bifidobacterium, which are known to suppress tumorigenesis
mtDam↑, Key constituents such as taraxasterol, chlorogenic acid, inulin, and various flavonoids exhibit synergistic effects that promote mitochondrial-mediated cell death, reduce oxidative stress, and preserve normal colonocyte function.
*ROS↓,
Casp1↑, DRE induces the upregulationof pro-apoptotic genes such as CASP1, TNF, TNFRSF1A, andSNCA, while downregulating anti-apoptotic regulators includingBCL2, BCL2A1, and PARP (PDF) Therapeutic Potential of Dandelion (Taraxacum officinale) Root Extract in
TNF-α↑,
Bcl-2↓,
PARP↓,
MMP↓, mitochondrial membrane depolarization, cytochrome c release, and caspase-3 activation have been confirmed following DRE treatment in CRC cells
Cyt‑c↓,
Casp3↑,
TumVol↓, DRE led to over 90% reduction in tumour volume without significant weight loss or systemic toxicity
COX2↓, taraxasterol has been shown to inhibit NF-κB nuclear translocation and block downstream activation of COX-2 and iNOS, contributing to an anti-inflammatory tumour microenvironment
iNOS↓,
ROS↑, revealed early mitochondrial membrane depolarization, followed by elevated ROS generation and activation of intrinsic apoptotic enzymes such as caspase 3 and caspase 8 in cancer cells effects not seen in NCM460 controls
selectivity↑,
TumCMig↓, RE significantly inhibits CRC cell migration and invasion, while normal epithelial cell motility remains intact.
TumCI↓,
ER Stress↑, One notable pathway involves the induction of EndoplasmicReticulum (ER) stress via activation of the PERK/eIF2α/ATF4/CHOP axis.
PERK↑,
eIF2α↑,
ATF4↑,
CHOP↑,
TumCCA↑, Treated TNBC cells displayed G2/M phase arrest associated with decreased levels of cyclin D1 and p21 and increased p53
cycD1/CCND1↓,
P21↓,
P53↑,
BioAv↝, Taraxasterol, alipophilic pentacyclic triterpenoid, shows poor oral bioavailability due to limited solubility and hepatic metabolism via CYP3A4enzymes.
Half-Life↝, Its analogs have half-lives ranging from 4-6 hr, with high plasma protein binding, suggesting a need for solubility-enhancing delivery systems such as liposomes or cyclodextrin complexes to improve bioavailability

2961- PL,    Piperlongumine inhibits esophageal squamous cell carcinoma in vitro and in vivo by triggering NRF2/ROS/TXNIP/NLRP3-dependent pyroptosis
- in-vitro, ESCC, KYSE-30
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↑,

37- QC,    Low Concentrations of Flavonoids Are Protective in Rat H4IIE Cells Whereas High Concentrations Cause DNA Damage and Apoptosis
- in-vivo, Hepat, H4IIE
DNAdamC↑,
Casp1↑,
BioAv↝, Published data on quercetin pharmacokinetics in humans suggest that a dietary supplement of 1–2 g of quercetin may result in plasma concentrations between 10 and 50 μmol/L


Showing Research Papers: 1 to 5 of 5

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 5

Pathway results for Effect on Cancer / Diseased Cells:


Redox & Oxidative Stress ⓘ

NRF2↓, 1,   OXPHOS↓, 1,   ROS↑, 3,   mt-ROS↑, 1,  

Mitochondria & Bioenergetics ⓘ

ETC↓, 1,   MMP↓, 2,   mtDam↑, 1,  

Cell Death ⓘ

p‑Akt↓, 1,   Apoptosis↑, 3,   Bcl-2↓, 2,   Bcl-2↑, 1,   BID↑, 1,   Casp1↑, 4,   cl‑Casp1↑, 1,   Casp3↑, 2,   Casp8↑, 1,   Cyt‑c↓, 1,   GSDMD↑, 1,   iNOS↓, 1,   Pyro↑, 1,   TumCD↑, 1,  

Protein Folding & ER Stress ⓘ

CHOP↑, 1,   eIF2α↑, 1,   ER Stress↑, 1,   PERK↑, 1,  

DNA Damage & Repair ⓘ

DNAdamC↑, 1,   P53↑, 1,   PARP↓, 2,  

Cell Cycle & Senescence ⓘ

cycD1/CCND1↓, 1,   P21↓, 1,   P21↑, 1,   TumCCA↑, 2,  

Proliferation, Differentiation & Cell State ⓘ

GSK‐3β↓, 1,   mTOR↓, 1,   PI3K↓, 1,   TumCG↓, 1,  

Migration ⓘ

E-cadherin↓, 1,   MMP2↓, 1,   MMP9↓, 1,   MMPs↓, 1,   TumCI↓, 2,   TumCMig↓, 3,   TumCP↓, 1,   TumMeta↓, 1,   TXNIP↑, 1,   β-catenin/ZEB1↓, 1,  

Angiogenesis & Vasculature ⓘ

ATF4↑, 1,   EGFR↓, 1,   Hif1a↓, 1,   VEGF↓, 1,  

Immune & Inflammatory Signaling ⓘ

ASC↑, 1,   COX2↓, 1,   COX2↑, 1,   NF-kB↓, 1,   NF-kB↑, 1,   TLR4↓, 1,   TNF-α↑, 1,  

Protein Aggregation ⓘ

NLRP3↑, 1,  

Drug Metabolism & Resistance ⓘ

BioAv↝, 2,   ChemoSen↑, 1,   Dose↝, 1,   eff↑, 1,   Half-Life↝, 1,   RadioS↑, 1,   selectivity↑, 3,  

Clinical Biomarkers ⓘ

EGFR↓, 1,  

Functional Outcomes ⓘ

toxicity↓, 1,   TumVol↓, 1,  
Total Targets: 68

Pathway results for Effect on Normal Cells:


Redox & Oxidative Stress ⓘ

GPx↑, 1,   lipid-P↓, 1,   NRF2↑, 1,   ROS↓, 3,   SOD↑, 1,  

Cell Death ⓘ

Casp1↓, 1,  

Immune & Inflammatory Signaling ⓘ

Inflam↓, 2,   NF-kB↓, 2,  

Synaptic & Neurotransmission ⓘ

AChE↓, 1,  

Protein Aggregation ⓘ

BACE↓, 1,  

Hormonal & Nuclear Receptors ⓘ

CYP19↓, 1,  

Drug Metabolism & Resistance ⓘ

BioAv↓, 1,  

Clinical Biomarkers ⓘ

ALP↓, 1,   AST↓, 1,   GutMicro↑, 1,  

Functional Outcomes ⓘ

AntiDiabetic↑, 1,   cardioP↑, 1,   hepatoP↑, 1,   memory↑, 1,   neuroP↑, 2,   Obesity↓, 1,   toxicity↓, 1,  

Infection & Microbiome ⓘ

Bacteria↓, 1,  
Total Targets: 23

Scientific Paper Hit Count for: Casp1, Caspase-1
2 Dandelion Root
1 Biochanin A
1 Piperlongumine
1 Quercetin
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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