GSDME-N Cancer Research Results

GSDME-N, N‐terminal domain of Gasdermin E: Click to Expand ⟱
Source:
Type:
GSDME‐N fragment (the N‐terminal domain of Gasdermin E)
• GSDME (Gasdermin E) is a member of the gasdermin family and is cleaved by caspase‐3 during apoptosis. This cleavage releases the N‐terminal fragment (GSDME‐N), which can form pores in the cell membrane, inducing pyroptosis—a proinflammatory form of programmed cell death.

• Some studies have found that high levels of GSDME expression, which can lead to increased GSDME‐N formation upon cleavage, correlate with enhanced pyroptosis in tumor cells.
• In select breast cancer cohorts, increased pyroptosis may contribute to a more robust local immune response, potentially correlating with improved prognosis.

- Formation of the GSDME‐N fragment and its associated induction of pyroptosis might, in some contexts, favor a more robust anti‐tumor immune response and potentially better clinical outcomes.
Scientific Papers found: Click to Expand⟱
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+↑,

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 2 of 2

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 2

Pathway results for Effect on Cancer / Diseased Cells:


Redox & Oxidative Stress ⓘ

NRF2↓, 1,   ROS?, 1,   ROS↑, 1,   xCT↓, 2,  

Mitochondria & Bioenergetics ⓘ

ATP↓, 1,   MMP↓, 1,   mtDam↑, 1,  

Core Metabolism/Glycolysis ⓘ

cMyc↓, 1,   GlucoseCon↓, 1,   Glycolysis↓, 1,   HK2↓, 1,   lactateProd↓, 1,  

Cell Death ⓘ

BAD↑, 1,   BAX↑, 2,   Bcl-2↓, 1,   Casp3↑, 1,   cl‑Casp3↑, 1,   Cyt‑c↑, 1,   GSDME-N↑, 2,   Pyro↑, 2,  

Transcription & Epigenetics ⓘ

tumCV?, 1,  

DNA Damage & Repair ⓘ

p‑P53↑, 1,  

Proliferation, Differentiation & Cell State ⓘ

TumCG↓, 1,  

Barriers & Transport ⓘ

CellMemb↓, 1,  

Immune & Inflammatory Signaling ⓘ

CD4+↑, 1,  

Drug Metabolism & Resistance ⓘ

eff↓, 1,   eff↑, 2,  

Functional Outcomes ⓘ

AntiCan↑, 1,  

Infection & Microbiome ⓘ

CD8+↑, 1,  
Total Targets: 29

Pathway results for Effect on Normal Cells:


Total Targets: 0

Scientific Paper Hit Count for: GSDME-N, N‐terminal domain of Gasdermin E
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#:1216  State#:%  Dir#:2
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