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⟱
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

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↓, 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 3 of 3

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 3

Pathway results for Effect on Cancer / Diseased Cells:


Redox & Oxidative Stress ⓘ

ROS↑, 1,   mt-ROS↑, 1,  

Core Metabolism/Glycolysis ⓘ

PDK1↓, 1,  

Cell Death ⓘ

Akt↓, 1,   Apoptosis↑, 2,   Bcl-2↓, 1,   Casp↑, 1,   Casp3↑, 1,   Casp9↑, 1,   Cyt‑c↑, 1,   GSDME↑, 1,   cl‑GSDME↑, 2,   Pyro↑, 3,  

DNA Damage & Repair ⓘ

cl‑PARP↑, 1,  

Cell Cycle & Senescence ⓘ

cycD1/CCND1↓, 1,   TumCCA↓, 1,  

Proliferation, Differentiation & Cell State ⓘ

ERK↓, 1,   TumCG↓, 2,  

Migration ⓘ

TumCP↓, 1,  

Immune & Inflammatory Signaling ⓘ

COX2↓, 1,   IL18↑, 1,   IL1β↑, 1,   NK cell↑, 1,  

Drug Metabolism & Resistance ⓘ

eff↓, 2,   eff↑, 2,  

Functional Outcomes ⓘ

AntiCan↑, 1,  
Total Targets: 26

Pathway results for Effect on Normal Cells:


Total Targets: 0

Scientific Paper Hit Count for: GSDME, gasdermin E
1 Honokiol
1 Magnolol
1 Baicalin
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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