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.
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Scientific Papers found: Click to Expand⟱
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in-vitro, |
Colon, |
HCT116 |
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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↓,
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.
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Review, |
Var, |
NA |
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Review, |
AD, |
NA |
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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↑,
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↑, 2,
Mitochondria & Bioenergetics ⓘ
CDC25↓, 1, MMP↑, 1,
Core Metabolism/Glycolysis ⓘ
AKT1↓, 1, lactateProd↓, 1,
Cell Death ⓘ
p‑Akt↓, 1, Apoptosis↑, 1, BAD↑, 1, Bak↑, 1, BAX↑, 1, Bcl-2↓, 1, Casp3↑, 1, proCasp3↓, 1, Casp8↓, 2, Casp8↑, 1, proCasp8↓, 1, Casp9↑, 1, proCasp9↓, 1, Cyt‑c↑, 1, Fas↑, 1, Myc↓, 1,
Protein Folding & ER Stress ⓘ
CHOP↑, 1, ER Stress↑, 1, GRP78/BiP↑, 1, UPR↑, 1,
Autophagy & Lysosomes ⓘ
ATG5↑, 1, Beclin-1↑, 1, LC3B↑, 1, LC3II↑, 1,
DNA Damage & Repair ⓘ
P53↑, 1, PARP↑, 1, cl‑PARP↑, 1, TP53↓, 1,
Cell Cycle & Senescence ⓘ
CycB/CCNB1↓, 1, P21↑, 1,
Proliferation, Differentiation & Cell State ⓘ
cDC2↓, 1, IGF-1R↑, 1, NOTCH3↓, 1, Wnt↑, 1,
Migration ⓘ
Zeb1↑, 1,
Angiogenesis & Vasculature ⓘ
ATF4↑, 1, VEGF↓, 1,
Drug Metabolism & Resistance ⓘ
eff↑, 2,
Clinical Biomarkers ⓘ
Myc↓, 1, TP53↓, 1,
Total Targets: 45
Pathway results for Effect on Normal Cells:
Redox & Oxidative Stress ⓘ
antiOx↑, 1, MPO↓, 1, ROS↓, 1,
Core Metabolism/Glycolysis ⓘ
glucose↓, 1, LDL↓, 1,
Cell Death ⓘ
BAX↓, 1, Cyt‑c↓, 1,
Migration ⓘ
Ca+2?, 1,
Immune & Inflammatory Signaling ⓘ
Inflam↓, 1, NF-kB↓, 1,
Functional Outcomes ⓘ
cardioP↑, 1, memory↑, 1, neuroP↑, 1,
Total Targets: 13
Scientific Paper Hit Count for: Casp8, CASP8, caspase 8, apoptosis-related cysteine peptidase
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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