Pyro Cancer Research Results

Pyro, Pyroptosis: Click to Expand ⟱
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Pyroptosis is a form of programmed cell death characterized by the formation of membrane pores by gasdermin proteins, leading to cell swelling, lysis, and the release of inflammatory mediators.
Scientific Papers found: Click to Expand⟱
2321- ART/DHA,    Dihydroartemisinin mediating PKM2-caspase-8/3-GSDME axis for pyroptosis in esophageal squamous cell carcinoma
- in-vitro, ESCC, Eca109 - in-vitro, ESCC, EC9706
Pyro↑, DHA treatment to ESCC, we found that some dying cells exhibited the characteristic morphology of pyroptosis, such as blowing large bubbles from the cell membrane,
PKM2↓, accompanied by downregulation of pyruvate kinase isoform M2 (PKM2),
Casp8↑, activation of caspase-8/3, and production of GSDME-NT
Casp3↑,
Warburg↓, previous studies, we demonstrated that DHA has anti-esophageal cancer effects by blocking the cell cycle in G0/G1 phase, inducing apoptosis, regulating the NF-κB/HIF-1α/VEGF pathway ... and downregulating the expression of PKM2 to inhibit the Warburg
TumCCA↑,
Apoptosis↑,

1572- Cu,    Recent Advances in Cancer Therapeutic Copper-Based Nanomaterials for Antitumor Therapy
- Review, NA, NA
eff↑, generate a large number of reactive oxygen species (ROS) when exposed to light, which could be adopted for photodynamic therapy.
Fenton↑, Cu2+ is vulnerable to the reduction to Cu+, allowing Cu to drive the Fenton reaction and produce hydroxyl radicals (·OH).
ROS↑, increasing Cu ions in cancer tissue makes an antitumor impact that mainly involves OS by triggering the Fenton reaction, which can produce ROS
eff↑, compared with other metals (iron, chromium, cobalt and nickel), the Cu-based Fenton reaction can react in wider pH range
mtDam↑, Excessive Cu can induce the toxic level of ROS that may aggravate the mitochondrial ROS, causing mitochondrial damage
BAX↑, Cu-induced ROS increased Bax (pro-apoptotic protein), while Bcl2 (anti-apoptotic protein) was decreased
Bcl-2↓,
MMP↓,
Cyt‑c↑, releasing CytC that activated Caspase3
Casp3↑,
ER Stress↑, Nano-CuO) triggers OS by ROS, thus stimulating endoplasmic reticulum (ER)-stress
CHOP↑, which thereby enhanced the expression of CHOP
Apoptosis↑, and CHOP-induced apoptosis
selectivity↑, In fact, autophagy induced by copper can either protect cells from death or contribute to cell death, depending on autophagic flux, which is associated with the concentration of copper.
eff↑, combining artemisinin (ART) and copper peroxide nanodots to enhance autophagy and ferroptosis that produced highly cancer toxic reaction
Pyro↑, Copper-Based Pyroptosis
Paraptosis↑, Copper-Based Paraptosis
Cupro↑, Copper-Based Cuproptosis
ChemoSen↑, studies suggested that Cu-MOFs might be a robust nanoplatform for enhancing chemotherapy activity of Cu-organic compounds.
eff↑, CuS NPs had the ability to directly target cancer cells and then induce in nucleus by modification of RGD and TAT peptides, thus heating cancer cell to exhaustive apoptosis through 980 nm NIR irradiation

5487- EP,    High-frequency irreversible electroporation improves survival and immune cell infiltration in rodents with malignant gliomas
- in-vivo, GBM, NA
OS↑, A statistically greater overall survival fraction was noted in the high-dose H-FIRE + liposomal doxorubicin
CellMemb↑, defects facilitate an increase in cell membrane permeability
Imm↑, non-thermal cell death mechanism induced by IRE can improve upon the antigen presentation and consequently the immune response
Inflam↓, cell death is in part pro-inflammatory (necrosis and pyroptosis),
necrosis↑,
Pyro↑,
eff↑, H-FIRE utilizes bursts of biphasic pulsed electric fields to non-thermally ablate neoplastic and non-neoplastic tissue while mitigating excitation of skeletal muscle and nerves during tissue ablation.
IL2↑, IFNγ, interleukin-2 (IL-2) (p< 0.01), interleukin-6 (IL-6) (p< 0.01), and interleukin-17a (IL-17a) (p< 0.001) were significantly elevated in rats treated with H-FIRE ablation
IL6↑,
IL17↑,
IFN-γ↓,

1959- GamB,    Gambogic acid induces GSDME dependent pyroptotic signaling pathway via ROS/P53/Mitochondria/Caspase-3 in ovarian cancer cells
- in-vitro, Ovarian, NA - in-vivo, NA, NA
AntiCan↑, Gambogic acid (GA) is a naturally active compound extracted from the Garcinia hanburyi with various anticancer activities.
Pyro↑, This study revealed that GA treatment reduced cell viability by inducing pyroptosis in OC cell lines
tumCV?,
CellMemb↓, loss of cell membrane integrity
cl‑Casp3↑, Cleaved caspase-3 and GSDME-N levels increased after GA treatment
GSDME-N↑,
ROS?, GA significantly increased reactive oxygen species (ROS) and p53 phosphorylation.
p‑P53↑,
eff↓, OC cells pretreated with ROS inhibitor N-Acetylcysteine (NAC) and the specific p53 inhibitor pifithrin-μ could completely reverse the pyroptosis post-treatment.
MMP↓, Elevated p53 and phosphorylated p53 reduced mitochondrial membrane potential (MMP) and Bcl-2
Bcl-2↓,
BAX↑,
mtDam↑, damage mitochondria by releasing cytochrome c to activate the downstream pyroptosis pathway
Cyt‑c↑,
TumCG↓, inhibited tumor growth in ID8 tumor-bearing mice
CD4+↑, high-dose GA increased in tumor-infiltrating lymphocytes CD3, CD4, and CD8 were detected in tumor tissues
CD8+↑,

2509- H2,    Hydrogen inhibits endometrial cancer growth via a ROS/NLRP3/caspase-1/GSDMD-mediated pyroptotic pathway
- in-vitro, Endo, AN3CA - in-vivo, Endo, NA
selectivity↑, Hydrogen exerts a biphasic effect on cancer by promoting tumor cell death and protecting normal cells, which might initiate GSDMD pathway-mediated pyroptosis.
mt-ROS↑, We therefore concluded that molecular hydrogen activated ROS and mtROS generation in endometrial cancer cells.
ROS↑,
TumW↓,
GSDMD↑, ability of hydrogen to stimulate NLRP3 inflammasome/GSDMD activation in pyroptosis
Pyro↑,
Dose↝, Hydrogenated water was produced by H2 dissolved in water saturantly under 0.4 MPa pressure for 6 h with a concentration of 1.0 ppm produced by hydrogen water apparatus
eff↓, In contrast, NAC decreased ROS levels in hydrogen-treated endometrial cancer cells
TumVol↓, We demonstrated that drinking hydrogen-rich water reduced the volume of endometrial tumors in a xenograft mouse model.

3787- H2,    Hydrogen, a Novel Therapeutic Molecule, Regulates Oxidative Stress, Inflammation, and Apoptosis
- Review, AD, NA
*Inflam↓, anti-inflammatory and antioxidant activity
*antiOx↑,
*ROS↓, annihilating excess reactive oxygen species production and modulating nuclear transcription factor.
*other↝, H2 does not explode if it is <10% when mixed with air or O2
*NF-kB↓, H2-rich saline inhibited the activation of crucial inflammatory signaling pathway NF-κB and reduced serum IL-1β, IL-6, and TNF-α levels,
*IL2↓,
*IL6↓,
*TNF-α↓,
*HO-1↑, Studies have demonstrated that H2 administration increased the HO-1 expression
Apoptosis↑, Similarly, cell apoptosis and autophagy were significantly enhanced in A549 and H1975 lung cancer cell lines treated with different concentrations of H2 gas
TumAuto↑,
*Sepsis↓, sepsis-related organ injury models, H2 treatment significantly reduced the expression of caspase-1 in the damaged organ and the levels of IL-1β and IL-18 cytokines
*NLRP3↓, NLRP3, caspase-1, and the N-terminal of gasdermin D (GSDMD-N), were reduced after lung inflation with 3% H2,
Pyro↑, H2-rich water inhibited the proliferation of endometrial cancer cells by triggering the NLRP3 inflammasome/caspase-1 mediated classical pyroptosis pathway and activated the downstream proinflammatory cytokine IL-1β.

4523- HNK,  MAG,  BA,    Honokiol-Magnolol-Baicalin Possesses Synergistic Anticancer Potential and Enhances the Efficacy of Anti-PD-1 Immunotherapy in Colorectal Cancer by Triggering GSDME-Dependent Pyroptosis
- in-vitro, CRC, HCT116 - in-vitro, CRC, LoVo - in-vivo, CRC, HCT116
AntiCan↑, honokiol (H), magnolol (M), and baicalin (B) are found to exhibit a synergistic anticancer effect on CRC
eff↑, Most importantly, HMB is shown to enhance the sensitivity of CRC cells to anti‐PD‐1 immunotherapy in vivo.
TumCP↓, HMB Synergistically Inhibits Cell Proliferation and Triggers Cell Death in CRC Cells and Organoid Models
TumCCA↓, HMB treatment induced G0/G1 phase arrest, accompanied by reduced expression of cyclin D1 and p‐RB expression in both HCT116 and LoVo cells.
cycD1/CCND1↓,
Pyro↑, HMB Synergistically Induces Pyroptosis and Apoptosis
Apoptosis↑,
cl‑GSDME↑, HMB Synergistically Induces Pyroptosis by Promoting the Cleavage of GSDME
Bcl-2↓, HMB treatment reduced Bcl‐2 expression, promoted cytochrome c release from mitochondria, and activated caspase‐9
Cyt‑c↑,
Casp9↑,
TumCG↓, results demonstrate that the HMB combination synergistically inhibited tumor growth and induced pyroptosis in vivo

5608- NaHCO3,    Sodium Bicarbonate Nanoparticles for Amplified Cancer Immunotherapy by Inducing Pyroptosis and Regulating Lactic Acid Metabolism
- Study, Var, NA
TumCG↓, Collectively, NaHCO3 NPs observably inhibit primary/distal tumor growth and tumor metastasis through acid neutralization remitted immunosuppression and pyroptosis induced immune activation
TumMeta↓,
e-pH↑,
Pyro↑,
Imm↑,
Na+↑, t can further release high amounts of Na+ ions inside tumor cells

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↑,

4966- PSO,    Psoralidin induces pyroptosis in both tumor cells and macrophages as well as enhances nature killer cell cytotoxicity to suppress hepatocellular carcinoma
- vitro+vivo, HCC, HepG2
Pyro↑, Psoralidin induced pyroptosis and GSDME cleavage in HepG2 and Hepa1–6 cells
TumCG↓, Psoralidin suppressed HCC growth, inducing tumor cell pyroptosis and enhancing the tumor infiltration of T cells and NK cells.
mt-ROS↑, psoralidin induced mitochondrial reactive oxygen species (ROS) production, leading to caspase-3 activation and subsequent GSDME cleavage.
Casp3↑,
cl‑GSDME↑,
IL1β↑, leading to the secretion of interleukin (IL)-1β and IL-18, which promoted natural killer (NK) cell activation
IL18↑,
NK cell↑,

2409- PTS,    Pterostilbene Induces Pyroptosis in Breast Cancer Cells through Pyruvate Kinase 2/Caspase-8/Gasdermin C Signaling Pathway
- in-vitro, BC, EMT6 - in-vitro, BC, 4T1 - in-vitro, Nor, HC11
Pyro↑, PTE induced pyroptosis by inhibiting tumor glycolysis
Glycolysis↓, demonstrated that PTE inhibited the glycolysis of tumor tissue.
*toxicity∅, we tested the toxicity of PTE to HC11. The result showed that PTE did not affect the viability of HC11 (p > 0.05, Figure 2G) and indicated that PTE was non-toxic to mouse mammary epithelial cells.
selectivity↑,
GSDMC↑, The above experiments had demonstrated that PTE activated GSDMC
PKM2↓, Our results showed that PTE down-regulated the expression of PKM2 and upregulate the expression of PKM1 in tumor cells
PKM1↑,
GlucoseCon↓, PTE induced pyroptosis in mouse breast xenografts. Colorimetric kit results showed that PTE down-regulated glucose consumption, lactate production, and ATP content
lactateProd↓,
ATP↓,
TumCG↓, PTE inhibits the growth of mouse breast xenografts in vivo.

2469- SK,    Shikonin induces the apoptosis and pyroptosis of EGFR-T790M-mutant drug-resistant non-small cell lung cancer cells via the degradation of cyclooxygenase-2
- in-vitro, Lung, H1975
Apoptosis↑, Shikonin induced cell apoptosis and pyroptosis by triggering the activation of the caspase cascade and cleavage of poly (ADP-ribose) polymerase and gasdermin E by elevating intracellular ROS levels
Pyro↑,
Casp↑,
cl‑PARP↑,
GSDME↑,
ROS↑,
COX2↓, shikonin induced the degradation of COX-2 via the proteasome pathway, thereby decreasing COX-2 protein level and enzymatic activity and subsequently inhibiting the downstream PDK1/Akt and Erk1/2 signaling pathways through the induction of ROS produc
PDK1↓,
Akt↓,
ERK↓,
eff↓, Notably, COX-2 overexpression attenuated shikonin-induced apoptosis and pyroptosis
eff↓, NAC pre-treatment inhibited the shikonin-induced activation of the caspase cascade (caspase-8/9/3) and cleavage of PARP and GSDME in H1975 cells
eff↑, Celecoxib augmented the cytotoxic effects of shikonin by promoting the apoptosis and pyroptosis of H1975 cells

2454- Trip,    Natural product triptolide induces GSDME-mediated pyroptosis in head and neck cancer through suppressing mitochondrial hexokinase-ΙΙ
- in-vitro, HNSCC, HaCaT - in-vivo, NA, NA
GSDME-N↑, Triptolide eliminates head and neck cancer cells through inducing gasdermin E (GSDME) mediated pyroptosis.
Pyro↑,
cMyc↓, TPL treatment suppresses expression of c-myc and mitochondrial hexokinase II (HK-II) in cancer cells
HK2↓,
BAD↑, leading to activation of the BAD/BAX-caspase 3 cascade and cleavage of GSDME by active caspase 3.
BAX↑,
Casp3↑,
NRF2↓, TPL treatment suppresses NRF2/SLC7A11 (also known as xCT) axis
xCT↓,
ROS↑, and induces reactive oxygen species (ROS) accumulation, regardless of the status of GSDME.
eff↑, Combination of TPL with erastin, an inhibitor of SLC7A11, exerts robust synergistic effect in suppression of tumor survival in vitro and in a nude mice model.
Glycolysis↓, TPL treatment repressed c-Myc/HK-II axis and aerobic glycolysis in head and neck cancer cells
GlucoseCon↓, as evidenced by reduced glucose consumption, lactate production and cellular ATP content following TPL treatment
lactateProd↓,
ATP↓,
xCT↓, TPL (50 nM) treatment decreased the protein levels of NRF2 and SLC7A11 (
eff↑, combination of TPL with erastin is a promising strategy for head and neck cancer therapy.


Showing Research Papers: 1 to 13 of 13

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 13

Pathway results for Effect on Cancer / Diseased Cells:


Redox & Oxidative Stress ⓘ

Fenton↑, 1,   NRF2↓, 2,   ROS?, 1,   ROS↑, 5,   mt-ROS↑, 2,   xCT↓, 2,  

Mitochondria & Bioenergetics ⓘ

ATP↓, 2,   MMP↓, 2,   mtDam↑, 2,  

Core Metabolism/Glycolysis ⓘ

cMyc↓, 1,   GlucoseCon↓, 2,   Glycolysis↓, 2,   HK2↓, 1,   lactateProd↓, 2,   PDK1↓, 1,   PKM1↑, 1,   PKM2↓, 2,   Warburg↓, 1,  

Cell Death ⓘ

Akt↓, 1,   Apoptosis↑, 5,   BAD↑, 1,   BAX↑, 3,   Bcl-2↓, 3,   Casp↑, 1,   cl‑Casp1↑, 1,   Casp3↑, 4,   cl‑Casp3↑, 1,   Casp8↑, 1,   Casp9↑, 1,   Cupro↑, 1,   Cyt‑c↑, 3,   GSDMC↑, 1,   GSDMD↑, 2,   GSDME↑, 1,   cl‑GSDME↑, 2,   GSDME-N↑, 2,   necrosis↑, 1,   Paraptosis↑, 1,   Pyro↑, 13,  

Transcription & Epigenetics ⓘ

tumCV?, 1,  

Protein Folding & ER Stress ⓘ

CHOP↑, 1,   ER Stress↑, 1,  

Autophagy & Lysosomes ⓘ

TumAuto↑, 1,  

DNA Damage & Repair ⓘ

p‑P53↑, 1,   cl‑PARP↑, 1,  

Cell Cycle & Senescence ⓘ

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

Proliferation, Differentiation & Cell State ⓘ

ERK↓, 1,   TumCG↓, 5,  

Migration ⓘ

Na+↑, 1,   TumCI↓, 1,   TumCMig↓, 1,   TumCP↓, 2,   TumMeta↓, 1,   TXNIP↑, 1,  

Barriers & Transport ⓘ

CellMemb↓, 1,   CellMemb↑, 1,   Na+↑, 1,  

Immune & Inflammatory Signaling ⓘ

ASC↑, 1,   CD4+↑, 1,   COX2↓, 1,   IFN-γ↓, 1,   IL17↑, 1,   IL18↑, 1,   IL1β↑, 1,   IL2↑, 1,   IL6↑, 1,   Imm↑, 2,   Inflam↓, 1,   NK cell↑, 1,  

Cellular Microenvironment ⓘ

e-pH↑, 1,  

Protein Aggregation ⓘ

NLRP3↑, 1,  

Drug Metabolism & Resistance ⓘ

ChemoSen↑, 1,   Dose↝, 1,   eff↓, 4,   eff↑, 9,   selectivity↑, 3,  

Clinical Biomarkers ⓘ

IL6↑, 1,  

Functional Outcomes ⓘ

AntiCan↑, 2,   OS↑, 1,   TumVol↓, 1,   TumW↓, 1,  

Infection & Microbiome ⓘ

CD8+↑, 1,  
Total Targets: 84

Pathway results for Effect on Normal Cells:


Redox & Oxidative Stress ⓘ

antiOx↑, 1,   HO-1↑, 1,   ROS↓, 1,  

Transcription & Epigenetics ⓘ

other↝, 1,  

Immune & Inflammatory Signaling ⓘ

IL2↓, 1,   IL6↓, 1,   Inflam↓, 1,   NF-kB↓, 1,   TNF-α↓, 1,  

Protein Aggregation ⓘ

NLRP3↓, 1,  

Clinical Biomarkers ⓘ

IL6↓, 1,  

Functional Outcomes ⓘ

toxicity∅, 1,  

Infection & Microbiome ⓘ

Sepsis↓, 1,  
Total Targets: 13

Scientific Paper Hit Count for: Pyro, Pyroptosis
2 Hydrogen Gas
1 Artemisinin
1 Copper and Cu NanoParticles
1 Electrical Pulses
1 Gambogic Acid
1 Honokiol
1 Magnolol
1 Baicalin
1 Bicarbonate(Sodium)
1 Piperlongumine
1 Psoralidin
1 Pterostilbene
1 Shikonin
1 triptolide
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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