CASP4 Cancer Research Results

CASP4, Caspase-4: Click to Expand ⟱
Source:
Type:

CASP4 - Caspase 4

Abbreviation: CASP4, Caspase-4

Type: Inflammatory caspase / cysteine protease / noncanonical inflammasome mediator / pyroptosis regulator

Function: Caspase-4 is a human inflammatory caspase that directly senses cytosolic lipopolysaccharide (LPS) and activates the noncanonical inflammasome pathway. Activated caspase-4 cleaves gasdermin D (GSDMD), generating the pore-forming GSDMD N-terminal fragment and promoting pyroptotic cell death. Caspase-4-mediated potassium efflux can also activate the NLRP3-caspase-1 pathway and enhance inflammatory cytokine release.

Cancer: ↕ Context-dependent. ↑ Caspase-4 activity can promote pyroptotic death of cancer cells and enhance antitumor immune responses. However, chronic caspase-4-dependent inflammation and pyroptosis-associated cytokine release can also create a tumor-promoting inflammatory microenvironment in some cancers.

Favorable Direction in Cancer: Context-dependent. ↑ CASP4 activity can be favorable when it induces tumor-cell pyroptosis, whereas ↓ CASP4-associated inflammatory signaling may be favorable where chronic inflammation promotes tumor progression.

Interpretation Note: Caspase-4 is distinct from apoptotic executioner caspases such as CASP3 and CASP7. In humans, CASP4 and CASP5 mediate noncanonical inflammasome signaling; murine CASP11 is the functional counterpart.
Scientific Papers found: Click to Expand⟱
8261- LCA,    Licochalcone A induces T24 bladder cancer cell apoptosis by increasing intracellular calcium levels
- in-vitro, CRC, T24/HTB-9
TumCP↓, Licochalcone A (LCA) has been reported to significantly inhibit cell proliferation, increase reactive oxygen species (ROS) levels, and induce apoptosis of T24 human bladder cancer cells via mitochondria and endoplasmic reticulum (ER) stress‑trigger
ROS↑,
Apoptosis↑,
ER Stress↑,
i-Ca+2↑, Treatment with LCA inhibited proliferation and induced apoptosis of T24 cells, and increased intracellular Ca2+ levels and ROS production.
MMP↓, LCA induced mitochondrial dysfunction, decreased mitochondrial membrane potential, and increased the mRNA expression levels of Apaf‑1, caspase‑9 and caspase‑3.
APAF1↑,
Casp9↑,
Casp3↑,
cal2↑, Exposure of T24 cells to LCA also triggered calpain 2 and caspase‑4 activation, resulting in apoptosis.
CASP4↑,


Showing Research Papers: 1 to 1 of 1

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 1

Pathway results for Effect on Cancer / Diseased Cells:


NA, unassigned(tgid=0) ⓘ

CASP4↑, 1,  

Redox & Oxidative Stress(tgid=1) ⓘ

ROS↑, 1,  

Mitochondria & Bioenergetics(tgid=3) ⓘ

MMP↓, 1,  

Cell Death(tgid=5) ⓘ

APAF1↑, 1,   Apoptosis↑, 1,   Casp3↑, 1,   Casp9↑, 1,  

Protein Folding & ER Stress(tgid=8) ⓘ

ER Stress↑, 1,  

Migration(tgid=13) ⓘ

i-Ca+2↑, 1,   cal2↑, 1,   TumCP↓, 1,  
Total Targets: 11

Pathway results for Effect on Normal Cells:


Total Targets: 0

Scientific Paper Hit Count for: CASP4, Caspase-4
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#:1792  State#:%  Dir#:2
  wNotes=on  sortOrder:rid,rpid

 

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