GSDME Cancer Research Results

GSDME, gasdermin E: Click to Expand ⟱
Source:
Type:
Gasdermin E (GSDME), also known as DFNA5

- GSDME is best known for its role in mediating pyroptosis, a form of inflammatory programmed cell death.

- In several cancers, GSDME is frequently silenced by promoter hypermethylation.
Scientific Papers found: Click to Expand⟱
6857- FBZ,    Fenbendazole induces pyroptosis in breast cancer cells through HK2/caspase-3/GSDME signaling pathway
- vitro+vivo, BC, NA
tumCV↓, In vitro, FBZ dose - dependently inhibited cell viability
Pyro↑, upregulated pyroptosis markers (cleaved caspase - 3, GSDME - NT, IL - 1β),
cl‑Casp3↑,
GSDME↑,
IL1β↑,
Glycolysis↓, suppressed glycolysis by downregulating HK2.
HK2↓,
TumVol↓, In vivo, FBZ treatment significantly reduced tumor volume and weight, with minimal systemic toxicity.
TumW↓,
toxicity↓,

7065- GamB,    Gambogic acid: A review of its pharmacological mechanisms against cancer
- Review, Var, NA
AntiTum↑, Preclinical studies demonstrate that GA exerts broad-spectrum antitumor effects through multiple mechanisms: induction of apoptosis via mitochondrial and death receptor pathways;
Apoptosis↑,
TumCCA↑, cell cycle arrest at G0/G1 or G2/M phases;
angioG↓, inhibition of angiogenesis via HIF-1α/VEGF/MMPs suppression;
Hif1a↓,
VEGF↓,
MMPs↓,
TumMeta↓, reduction of metastasis through downregulation of MMPs.
NF-kB↓, GA modulates key oncogenic pathways including NF-κB, PI3K/Akt/mTOR, and MAPKs. Several studies report an inhibitory effect of GA on NF-κB signaling
PI3K↓, inhibiting the phosphorylation (activation) of Akt and mTOR, thereby suppressing the PI3K/Akt/mTOR signaling cascade
Akt↓,
mTOR↓,
MAPK↓, this study linked the anti-invasive effect to the inhibition of MAPK signaling
P-gp/ABCB1↓, targeting P-glycoprotein, Bcr-Abl, and SHH pathways. This dual action of inhibiting both P-gp function/expression and a key signaling pathway (NF-κB) driving resistance makes GA a particularly attractive agent for tackling MDR.
Shh↓, GA’s downregulation of the SHH signaling pathway
Pyro↑, GA induces immunogenic pyroptosis via caspase-3/GSDME activation
Casp3↑,
GSDME↑,
ChemoSen↑, Synergistic effects are observed when GA is combined with chemotherapy, targeted agents (e.g., bortezomib, gefitinib), radiotherapy, or photothermal therapy.
RadioS↑,
BioAv↓, However, GA’s clinical application is limited by poor solubility and bioavailability.
Bcl-2↓, decrease in the expression of anti-apoptotic proteins like Bcl-2 and Mcl-1, coupled with an increase in pro-apoptotic proteins like Bax,
Mcl-1↓,
BAX↑,
Half-Life↓, GA can exhibit a short half-life in circulation, limiting its exposure time at the tumor site
ROS↑, As mentioned earlier, the generation of reactive oxygen species (ROS) appears to be a significant factor in GA’s action in multiple cancer types
miR-21↓, GA treatment counteracted this process; it reduced miR-21 levels in tumor cells
MMP2↓, GA decreased both the protein levels (Western blotting, immunocytochemistry) and the enzymatic activities (gelatin zymography) of MMP-2 and MMP-9.
MMP9↓,

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

7771- IBC,    Isobavachalcone induces concurrent apoptosis and pyroptosis in anaplastic thyroid cancer cells by modulating the caspase-mediated cleavage of PARP and GSDME
- vitro+vivo, Thyroid, CAL-62
TumCG↓, IBC inhibits ATC cell growth by inducing cell cycle arrest in the G2/M and S phases. IBC induces apoptosis and pyroptosis, with caspase-dependent Poly ADP-ribose Polymerase (PARP) and Gasdermin E (GSDME) cleavage simultaneously.
TumCCA↑,
Apoptosis↑,
Pyro↑,
Casp↑,
cl‑PARP↑,
cl‑GSDME↑,
TrxR1↓, Mechanistic studies have shown that IBC targets the selenocysteine-containing antioxidant enzyme thioredoxin reductase 1 (TrxR1), inhibiting its activity and leading excessive accumulation of reactive oxygen species (ROS).
ROS↑,
ER Stress↑, This ROS overload subsequently triggers endoplasmic reticulum (ER) stress and induces mitochondria-mediated apoptosis
Dose↝, 57.10 μM for 8505C, 51.10 μM for BHT-101, 65.27 μM for KHM-5M, 56.30 μM for C643, and 79.29 μM for Hth-7 cells

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↑,

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/PTGS2↓, 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


Showing Research Papers: 1 to 6 of 6

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 6

Pathway results for Effect on Cancer / Diseased Cells:


Redox & Oxidative Stress(tgid=1) ⓘ

ROS↑, 3,   mt-ROS↑, 1,   TrxR1↓, 1,  

Core Metabolism/Glycolysis(tgid=4) ⓘ

Glycolysis↓, 1,   HK2↓, 1,   PDK1↓, 1,  

Cell Death(tgid=5) ⓘ

Akt↓, 2,   Apoptosis↑, 4,   BAX↑, 1,   Bcl-2↓, 2,   Casp↑, 2,   Casp3↑, 2,   cl‑Casp3↑, 1,   Casp9↑, 1,   Cyt‑c↑, 1,   GSDME↑, 3,   cl‑GSDME↑, 3,   MAPK↓, 1,   Mcl-1↓, 1,   Pyro↑, 6,  

Transcription & Epigenetics(tgid=7) ⓘ

miR-21↓, 1,   tumCV↓, 1,  

Protein Folding & ER Stress(tgid=8) ⓘ

ER Stress↑, 1,  

DNA Damage & Repair(tgid=10) ⓘ

cl‑PARP↑, 2,  

Cell Cycle & Senescence(tgid=11) ⓘ

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

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

ERK↓, 1,   mTOR↓, 1,   PI3K↓, 1,   Shh↓, 1,   TumCG↓, 3,  

Migration(tgid=13) ⓘ

MMP2↓, 1,   MMP9↓, 1,   MMPs↓, 1,   TumCP↓, 1,   TumMeta↓, 1,  

Angiogenesis & Vasculature(tgid=14) ⓘ

angioG↓, 1,   Hif1a↓, 1,   VEGF↓, 1,  

Barriers & Transport(tgid=15) ⓘ

P-gp/ABCB1↓, 1,  

Immune & Inflammatory Signaling(tgid=16) ⓘ

COX2/PTGS2↓, 1,   IL18↑, 1,   IL1β↑, 2,   NF-kB↓, 1,   NK cell↑, 1,  

Drug Metabolism & Resistance(tgid=21) ⓘ

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

Functional Outcomes(tgid=23) ⓘ

AntiCan↑, 1,   AntiTum↑, 1,   toxicity↓, 1,   TumVol↓, 1,   TumW↓, 1,  
Total Targets: 58

Pathway results for Effect on Normal Cells:


Total Targets: 0

Scientific Paper Hit Count for: GSDME, gasdermin E
1 Fenbendazole
1 Gambogic Acid
1 Honokiol
1 Magnolol
1 Baicalin
1 Isobavachalcone
1 Psoralidin
1 Shikonin
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#:1311  State#:%  Dir#:2
  wNotes=on  sortOrder:rid,rpid

 

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