Casp8 Cancer Research Results

Casp8, CASP8, caspase 8, apoptosis-related cysteine peptidase: Click to Expand ⟱
Source: CGL-Driver Genes
Type: TSG
Caspase-8 is a unique member of caspases with a dual role in cell death and survival. Caspase-8 expression is often lost in some tumors, but increased in others, indicating a potential pro-survival function in cancer.
Caspase-8 (Casp8) acts as an initiator in cell apoptosis signaling. However, the role of Casp8 in tuning the tumor immune microenvironment remains controversial due to the complicated crosstalk between immune-tolerogenic apoptotic cell death and immunogenic cell death cascades.
Scientific Papers found: Click to Expand⟱
173- Api,    Apigenin-induced apoptosis is enhanced by inhibition of autophagy formation in HCT116 human colon cancer cells
- in-vitro, Colon, HCT116
CycB/CCNB1↓,
cDC2↓,
CDC25↓,
P53↑,
P21↑,
cl‑PARP↑, cleavage
proCasp8↓, Apigenin induced poly (ADP-ribose) polymerase (PARP) cleavage and decreased the levels of procaspase-8, -9 and -3
proCasp9↓,
proCasp3↓,

6069- CHL,  PDT,    Anti-Cancer Effect of Chlorophyllin-Assisted Photodynamic Therapy to Induce Apoptosis through Oxidative Stress on Human Cervical Cancer
- in-vitro, Cerv, HeLa
eff↑, chlorophyllin-assisted photodynamic therapy significantly induced cytotoxicity
ROS↑, In addition, reactive oxygen species generation and Annexin V expression level were detected on the photodynamic reaction-treated HeLa cells under the optimized conditions to evaluate apoptosis using a fluorescence microscope.
Casp8↓, the photodynamic therapy group showed the increased protein expression level of the cleaved caspase 8, caspase 9, Bax, and cytochrome C, and the suppressed protein expression level of Bcl-2, pro-caspase 8, and pro-caspase 9.
Casp9↑,
BAX↑,
Cyt‑c↑,
Bcl-2↓,
AKT1↓, the proposed photodynamic therapy downregulated the phosphorylation of AKT1 in the HeLa cells.

6342- DRE,    Mechanistic Study on the Inhibitory Effect of Dandelion Extract on Breast Cancer Cell Proliferation and Its Induction of Apoptosis
- in-vitro, BC, MDA-MB-231 - in-vitro, Nor, MCF10
eff↑, MTT assays revealed that the ethyl acetate fraction exhibited the strongest inhibitory effect on cell proliferation.
selectivity↑, 12 potential active compounds, including sesquiterpenes such as Isoalantolactone and Artemisinin, which showed significantly lower toxicity toward normal mammary epithelial MCF-10A cells compared to tumor cells (
Apoptosis↑, the extract induced apoptosis in a dose-dependent manner, with an apoptosis rate as high as 85.04%, and significantly arrested the cell cycle at the S and G2/M phases
TumCCA↑,
PI3K↓, antitumor effects were primarily mediated through the regulation of PI3K-Akt (hsa04151), JAK-STAT (hsa04630), and PPAR (hsa03320) signaling pathways.
Akt↓, these active compounds exhibited strong binding affinities with key target proteins such as PI3K and JAK1
JAK1↓,
STAT↓,
PPARγ↑, EA-2 may remodel tumor cell lipid metabolism by activating the PPARγ pathway
TumCP↓, EA-2 Inhibits the Proliferation of MDA-MB-231 Breast Cancer Cells In Vitro
SIRT6↓, PI3K, AKT1S1, SIRT6, JAK1, SCD, STAT3, CASP8, STAT6, PAK1, and FABP4—were significantly downregulated.
SCD1↓,
STAT3↓,
Casp8↓,
STAT6↓,
PAK1↓,
FABP4↓,

3205- EGCG,    The Role of Epigallocatechin-3-Gallate in Autophagy and Endoplasmic Reticulum Stress (ERS)-Induced Apoptosis of Human Diseas
- Review, Var, NA - Review, AD, NA
Beclin-1↑, EGCG not only regulates autophagy via increasing Beclin-1 expression and reactive oxygen species generation,
ROS↑,
Apoptosis↑, Apoptosis is a common cell function in biology and is induced by endoplasmic reticulum stress (ERS)
ER Stress↑,
*Inflam↓, EGCG has health benefits including anti-tumor [15], anti-inflammatory [16], anti-diabetes [17], anti-myocardial infarction [18], anti-cardiac hypertrophy [19], anti-atherosclerosis [20], and antioxidant
*cardioP↑,
*antiOx↑,
*LDL↓, These effects are mainly related to (LDL) cholesterol inhibition, NF-κB inhibition, MPO activity inhibition, decreased levels of glucose and glycated hemoglobin in plasma, decreased inflammatory markers, and reduced ROS generation
*NF-kB↓,
*MPO↓,
*glucose↓,
*ROS↓,
ATG5↑, EGCG induced autophagy by enhancing Beclin-1, ATG5, and LC3B and promoted mitochondrial depolarization in breast cancer cells.
LC3B↑,
MMP↑,
lactateProd↓, 20 mg kg−1 EGCG significantly decreased glucose, lactic acid, and vascular endothelial growth factor (VEGF) levels
VEGF↓,
Zeb1↑, (20 uM) inhibited the proliferation through activating autophagy via upregulating ZEB1, WNT11, IGF1R, FAS, BAK, and BAD genes and inhibiting TP53, MYC, and CASP8 genes in SSC-4 human oral squamous cells [
Wnt↑,
IGF-1R↑,
Fas↑,
Bak↑,
BAD↑,
TP53↓,
Myc↓,
Casp8↓,
LC3II↑, increasing the LC3-II expression levels and induced apoptosis via inducing ROS in mesothelioma cell lines,
NOTCH3↓, but also could reduce partially Notch3/DLL3 to reduce drug-resistance and the stemness of tumor cells
eff↑, In combination therapies, low-intensity pulsed electric field (PEF) can improve EGCG to affect tumor cells; ultrasound (US) with tumor cells is the application of physical stimulation in cancer therapy.
p‑Akt↓, 20 μM EGCG increased intracellular ROS levels and LC3-II, and inhibited p-Akt in PANC-1 cells
PARP↑, 100 μM EGCG increased LC3-II, activated caspase-3 and PARP, and reduced p-Akt in HepG2
*Cyt‑c↓, EGCG protected neuronal cells against human viruses by inhibiting cytochrome c and Bax translocations, and reducing autophagy with increased LC3-II expression and decreased p62 expression
*BAX↓,
*memory↑, EGCG restored autophagy in the mTOR/p70S6K pathway to weaken memory and learning disorders induced by CUMS
*neuroP↑, Finally, EGCG increased the neurological scores through inhibiting cell death
*Ca+2?, EGCG treatment, [Ca2+]m and [Ca2+]i expressions were reduced and oxyhemoglobin-induced mitochondrial dysfunction lessened.
GRP78/BiP↑, MMe cells with EGCG treatment improved GRP78 expression in the endoplasmic reticulum, and induced EDEM, CHOP, XBP1, and ATF4 expressions, and increased the activity of caspase-3 and caspase-8.
CHOP↑, GRP78 accumulation converted UPR of MMe cells into pro-apoptotic ERS
ATF4↑,
Casp3↑,
Casp8↑,
UPR↑,

6442- SAO,    Medicinal properties of alpha-santalol, a naturally occurring constituent of sandalwood oil: review
- Review, RCC, NA
AntiTum↑, the antitumour and cancer preventive properties of alpha-santalol have been shown to involve cell death induction through apoptosis and cell cycle arrest in various cancer models.
Apoptosis↑,
TumCCA↑,
*Inflam↓, marked decrease in inflammatory markers have also been shown with alpha-santalol administration in skin tissue models
selectivity↑, regarding its toxicity, it was concluded that alpha-santalol is less toxic to normal breast epithelial cells (MCF-10A) than to breast cancer cells (MCF-7) (
tumCV↓, proliferation of both cell lines was reduced, but viability was decreased only in cancer cells.
Casp8↓, alpha-santalol induced extrinsic and intrinsic pathways of apoptosis in both cells with activation of caspase-8, 9 and cause dactivation of the executioner caspase-6, 7 in MCF-7 cells and caspase-3, and 6 in MDA-MB-231 cells along with PARP cleavage
Casp9↓,
Casp6↓,
Casp3↓,
cl‑PARP↑,
angioG↓, alpha-santalol inhibits angiogenesis by targeting VEGFR2 regulated AKT/mTOR/P70S6 K signalling pathway and as a result, suppresses tumour growth
VEGFR2↓,
Akt↑,
mTOR↓,
TumCG↓,
*GSTs↑, sandalwood oil on liver function by measuring the activity of glutathione S-transferase (GST) and levels of soluble sulphyduryl found that feeding of 5 μL of sandalwood oil to mice for 10 and 20 days produced a 1.80 and 1.93-fold increase in GST
*antiOx↑, antioxidant and free radical scavenging effects are well documented with methanolic extracts of sandalwood at different doses
*ROS↓,


Showing Research Papers: 1 to 5 of 5

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 5

Pathway results for Effect on Cancer / Diseased Cells:


Redox & Oxidative Stress(tgid=1) ⓘ

ROS↑, 2,  

Mitochondria & Bioenergetics(tgid=3) ⓘ

CDC25↓, 1,   MMP↑, 1,  

Core Metabolism/Glycolysis(tgid=4) ⓘ

AKT1↓, 1,   FABP4↓, 1,   lactateProd↓, 1,   PPARγ↑, 1,   SCD1↓, 1,  

Cell Death(tgid=5) ⓘ

Akt↓, 1,   Akt↑, 1,   p‑Akt↓, 1,   Apoptosis↑, 3,   BAD↑, 1,   Bak↑, 1,   BAX↑, 1,   Bcl-2↓, 1,   Casp3↓, 1,   Casp3↑, 1,   proCasp3↓, 1,   Casp6↓, 1,   Casp8↓, 4,   Casp8↑, 1,   proCasp8↓, 1,   Casp9↓, 1,   Casp9↑, 1,   proCasp9↓, 1,   Cyt‑c↑, 1,   Fas↑, 1,   Myc↓, 1,  

Transcription & Epigenetics(tgid=7) ⓘ

tumCV↓, 1,  

Protein Folding & ER Stress(tgid=8) ⓘ

CHOP↑, 1,   ER Stress↑, 1,   GRP78/BiP↑, 1,   UPR↑, 1,  

Autophagy & Lysosomes(tgid=9) ⓘ

ATG5↑, 1,   Beclin-1↑, 1,   LC3B↑, 1,   LC3II↑, 1,  

DNA Damage & Repair(tgid=10) ⓘ

P53↑, 1,   PARP↑, 1,   cl‑PARP↑, 2,   SIRT6↓, 1,   TP53↓, 1,  

Cell Cycle & Senescence(tgid=11) ⓘ

CycB/CCNB1↓, 1,   P21↑, 1,   TumCCA↑, 2,  

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

cDC2↓, 1,   IGF-1R↑, 1,   mTOR↓, 1,   NOTCH3↓, 1,   PI3K↓, 1,   STAT↓, 1,   STAT3↓, 1,   STAT6↓, 1,   TumCG↓, 1,   Wnt↑, 1,  

Migration(tgid=13) ⓘ

PAK1↓, 1,   TumCP↓, 1,   Zeb1↑, 1,  

Angiogenesis & Vasculature(tgid=14) ⓘ

angioG↓, 1,   ATF4↑, 1,   VEGF↓, 1,   VEGFR2↓, 1,  

Immune & Inflammatory Signaling(tgid=16) ⓘ

JAK1↓, 1,  

Drug Metabolism & Resistance(tgid=21) ⓘ

eff↑, 3,   selectivity↑, 2,  

Clinical Biomarkers(tgid=22) ⓘ

Myc↓, 1,   TP53↓, 1,  

Functional Outcomes(tgid=23) ⓘ

AntiTum↑, 1,  
Total Targets: 69

Pathway results for Effect on Normal Cells:


Redox & Oxidative Stress(tgid=1) ⓘ

antiOx↑, 2,   GSTs↑, 1,   MPO↓, 1,   ROS↓, 2,  

Core Metabolism/Glycolysis(tgid=4) ⓘ

glucose↓, 1,   LDL↓, 1,  

Cell Death(tgid=5) ⓘ

BAX↓, 1,   Cyt‑c↓, 1,  

Migration(tgid=13) ⓘ

Ca+2?, 1,  

Immune & Inflammatory Signaling(tgid=16) ⓘ

Inflam↓, 2,   NF-kB↓, 1,  

Functional Outcomes(tgid=23) ⓘ

cardioP↑, 1,   memory↑, 1,   neuroP↑, 1,  
Total Targets: 14

Scientific Paper Hit Count for: Casp8, CASP8, caspase 8, apoptosis-related cysteine peptidase
1 Apigenin (mainly Parsley)
1 Chlorophyllin
1 Photodynamic Therapy
1 Dandelion Root
1 EGCG (Epigallocatechin Gallate)
1 α-Santalol/Sandalwood oil
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#:44  State#:%  Dir#:1
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