Casp3 Cancer Research Results

Casp3, CPP32, Cysteinyl aspartate specific proteinase-3: Click to Expand ⟱
Source:
Type:
Also known as CP32.
Cysteinyl aspartate specific proteinase-3 (Caspase-3) is a common key protein in the apoptosis and pyroptosis pathways, and when activated, the expression level of tumor suppressor gene Gasdermin E (GSDME) determines the mechanism of tumor cell death.
As a key protein of apoptosis, caspase-3 can also cleave GSDME and induce pyroptosis. Loss of caspase activity is an important cause of tumor progression.
Many anticancer strategies rely on the promotion of apoptosis in cancer cells as a means to shrink tumors. Crucial for apoptotic function are executioner caspases, most notably caspase-3, that proteolyze a variety of proteins, inducing cell death. Paradoxically, overexpression of procaspase-3 (PC-3), the low-activity zymogen precursor to caspase-3, has been reported in a variety of cancer types. Until recently, this counterintuitive overexpression of a pro-apoptotic protein in cancer has been puzzling. Recent studies suggest subapoptotic caspase-3 activity may promote oncogenic transformation, a possible explanation for the enigmatic overexpression of PC-3. Herein, the overexpression of PC-3 in cancer and its mechanistic basis is reviewed; collectively, the data suggest the potential for exploitation of PC-3 overexpression with PC-3 activators as a targeted anticancer strategy.
Caspase 3 is the main effector caspase and has a key role in apoptosis. In many types of cancer, including breast, lung, and colon cancer, caspase-3 expression is reduced or absent.
On the other hand, some studies have shown that high levels of caspase-3 expression can be associated with a better prognosis in certain types of cancer, such as breast cancer. This suggests that caspase-3 may play a role in the elimination of cancer cells, and that therapies aimed at activating caspase-3 may be effective in treating certain types of cancer.
Procaspase-3 is a apoptotic marker protein.
Prognostic significance:
• High Cas3 expression: Associated with good prognosis and increased sensitivity to chemotherapy in breast, gastric, lung, and pancreatic cancers.
• Low Cas3 expression: Linked to poor prognosis and increased risk of recurrence in colorectal, hepatocellular carcinoma, ovarian, and prostate cancers.
ESCC, Oesophageal Squamous Cell Carcinoma: Click to Expand ⟱
Esophageal cancer is a growth of cells that starts in the esophagus.
Scientific Papers found: Click to Expand⟱
251- AL,    Inhibition of allicin in Eca109 and EC9706 cells via G2/M phase arrest and mitochondrial apoptosis pathway
- in-vitro, ESCC, Eca109 - in-vitro, ESCC, EC9706 - in-vivo, NA, NA
Apoptosis↑, P53↑, P21↑, CHK1↑, CycB/CCNB1↓, BAX↑, Casp3↑, Casp9↑, Cyt‑c↑,
2323- ART/DHA,    Dihydroartemisinin represses esophageal cancer glycolysis by down-regulating pyruvate kinase M2
- in-vitro, ESCC, Eca109 - in-vitro, ESCC, EC9706
PKM2↓, lactateProd↓, GlucoseCon↓, cycD1/CCND1↓, Bcl-2↓, MMP2↓, VEGF↓, Casp3↑, cl‑PARP↑, BAX↑, DNAdam↑, ROS↑,
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↑, PKM2↓, Casp8↑, Casp3↑, Warburg↓, TumCCA↑, Apoptosis↑,
2805- CHr,    Chrysin serves as a novel inhibitor of DGKα/FAK interaction to suppress the malignancy of esophageal squamous cell carcinoma (ESCC)
- in-vitro, ESCC, KYSE150 - in-vivo, ESCC, NA
FAK↓, GlucoseCon↓, Casp3↑, Casp7↑, p‑Akt↓, TumCG↓, Weight∅,
5151- GamB,    Gambogic acid affects ESCC progression through regulation of PI3K/AKT/mTOR signal pathway
- in-vitro, ESCC, KYSE-30 - in-vitro, ESCC, KYSE450
TumCP↓, TumCMig↓, TumCI↓, Apoptosis↑, Bcl-2↓, BAX↑, cl‑PARP1↑, cl‑Casp3↑, cl‑Casp9↑, PI3K↓, p‑Akt↓, p‑mTOR↓, PTEN↑,
4527- MAG,    Magnolol inhibits growth and induces apoptosis in esophagus cancer KYSE-150 cell lines via the MAP kinase pathway
- in-vitro, ESCC, TE1 - in-vitro, ESCC, Eca109 - vitro+vivo, SCC, KYSE150
TumCP↓, TumCMig↓, MMP2↓, Apoptosis↑, cl‑Casp3↑, cl‑Casp9↑, BAX↑, Bcl-2↓, p‑p38↓, TumCG↓,
2232- SK,    Shikonin Induces Autophagy and Apoptosis in Esophageal Cancer EC9706 Cells by Regulating the AMPK/mTOR/ULK Axis
- in-vitro, ESCC, EC9706
tumCV↓, TumCMig↓, TumCI↓, TumAuto↑, Apoptosis↑, Bcl-2↓, BAX↑, cl‑Casp3↑, cl‑Casp8↑, cl‑PARP↑, AMPK↑, mTOR↑, TumVol↓, OS↑, LC3I↑,

Showing Research Papers: 1 to 7 of 7

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 7

Pathway results for Effect on Cancer / Diseased Cells:


Redox & Oxidative Stress ⓘ

ROS↑, 1,  

Core Metabolism/Glycolysis ⓘ

AMPK↑, 1,   GlucoseCon↓, 2,   lactateProd↓, 1,   PKM2↓, 2,   Warburg↓, 1,  

Cell Death ⓘ

p‑Akt↓, 2,   Apoptosis↑, 5,   BAX↑, 5,   Bcl-2↓, 4,   Casp3↑, 4,   cl‑Casp3↑, 3,   Casp7↑, 1,   Casp8↑, 1,   cl‑Casp8↑, 1,   Casp9↑, 1,   cl‑Casp9↑, 2,   Cyt‑c↑, 1,   p‑p38↓, 1,   Pyro↑, 1,  

Transcription & Epigenetics ⓘ

tumCV↓, 1,  

Autophagy & Lysosomes ⓘ

LC3I↑, 1,   TumAuto↑, 1,  

DNA Damage & Repair ⓘ

CHK1↑, 1,   DNAdam↑, 1,   P53↑, 1,   cl‑PARP↑, 2,   cl‑PARP1↑, 1,  

Cell Cycle & Senescence ⓘ

CycB/CCNB1↓, 1,   cycD1/CCND1↓, 1,   P21↑, 1,   TumCCA↑, 1,  

Proliferation, Differentiation & Cell State ⓘ

mTOR↑, 1,   p‑mTOR↓, 1,   PI3K↓, 1,   PTEN↑, 1,   TumCG↓, 2,  

Migration ⓘ

FAK↓, 1,   MMP2↓, 2,   TumCI↓, 2,   TumCMig↓, 3,   TumCP↓, 2,  

Angiogenesis & Vasculature ⓘ

VEGF↓, 1,  

Functional Outcomes ⓘ

OS↑, 1,   TumVol↓, 1,   Weight∅, 1,  
Total Targets: 46

Pathway results for Effect on Normal Cells:


Total Targets: 0

Scientific Paper Hit Count for: Casp3, CPP32, Cysteinyl aspartate specific proteinase-3
2 Artemisinin
1 Allicin (mainly Garlic)
1 Chrysin
1 Gambogic Acid
1 Magnolol
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:41  Cells:%  prod#:%  Target#:42  State#:%  Dir#:2
  wNotes=0  sortOrder:rid,rpid

 

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