Casp Cancer Research Results

Casp, caspase: Click to Expand ⟱
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The caspase family of proteases are essential to initiate and execute apoptotic cell death. Targeting caspase pathways by gene therapy or endogenous inhibitors represents a promising therapeutic strategy for cancer.
Caspases are divided into two groups: the initiator caspases (caspase-2, -8, -9 and -10), which are the first to be activated in response to a signal, and the executioner caspases (caspase-3, -6, and -7) that carry out the demolition phase of apoptosis.
Caspases are a cysteine protease that speed up a chemical reaction via pointing their target substrates following an aspartic acid residue.1 They are grouped into apoptotic (caspase-2, 3, 6, 7, 8, 9 and 10) and inflammatory (caspase-1, 4, 5, 11 and 12) mediated caspases.
Scientific Papers found: Click to Expand⟱
810- GAR,  GEM,    Garcinol sensitizes human pancreatic adenocarcinoma cells to gemcitabine in association with microRNA signatures
- in-vitro, PC, NA
TumCP↓, Garcinol synergizes with gemcitabine to inhibit cell proliferation and induce apoptosis
Apoptosis↑,
PARP↝,
VEGF↝,
MMPs↝,
Casp↝,
NF-kB↝,
miR-21↝,

6562- Ger,    Potential Effects of Geraniol on Cancer and Inflammation-Related Diseases: A Review of the Recent Research Findings
- Review, Var, NA - Review, AD, NA
*Inflam↓, wide spectrum of pharmacological activities including anti-inflammatory, anticancer, antimicrobial, antioxidant, and neuroprotective activities.
*AntiCan↑,
*AntiBio↑,
*antiOx↑,
*neuroP↑,
ROS↓, GNL scavenges free radicals and preserves the activity of antioxidant enzymes.
Apoptosis↑, GNL induces apoptosis and cell cycle arrest, modulates multiple molecular targets, including p53 and STAT3, activates caspases, and modulates inflammation via transcriptional regulation.
TumCCA↑,
P53↝,
STAT3↓, GNL reduces survivin protein levels by downregulating phosphorylated STAT3.
Casp↝,
*Catalase↑, This compound protects various antioxidant enzymes, such as catalase, glutathione-S-transferase, and glutathione peroxidase.
*GSTs↑,
*GPx↑,
*AChE↓, In addition, GNL suppressed acetylcholinesterase (AChE) activity and alleviated oxidative stress by boosting neuronal reduced glutathione (GSH), catalase (CAT), glutathione-S-transferase (GST), and superoxide dismutase (SOD) activities.
*GSH↑,
*SOD↑,
*TBARS↓, It lowered malondialdehyde concentration (TBARS), nitric oxide (NO), and xanthine oxidase (XO), and restored the structural damage to the brain tissue caused by HFD.
*NO↓,
*XO↓,
*memory↑, GNL boosted learning and memory function and ameliorated the inflammation status in the brain by lowering the protein levels of IL-1β, iNOS, NF-κBp65, and COX-2
*IL1β↓,
*iNOS↓,
*NF-kB↓,
*COX2↓,
*NRF2↑, GNL administration ameliorated renal function, alleviated histological changes, and enhanced Nrf-2/HO-1/NQO-1 with a subsequent intensification of antioxidant enzyme activities.
*HO-1↑,
*survivin↓, GNL reduces survivin protein levels by downregulating phosphorylated STAT3.
TumCP↓, They have shown that GNL treatment significantly suppressed oral squamous cell carcinoma (OSCC) cell proliferation and migration in vitro and tumor growth in vivo in a time- and dose-dependent manner.
TumCMig↓,
TumCG↑,
selectivity↑, GNL may be helpful in treating different types of malignancy, while having limited effects on normal cells.
TumMeta↓, GNL has been reported to inhibit cancer metastasis and angiogenesis.
angioG↓,
Hif1a↓, A549 lung cancer cells treated with GNL, downregulation of HIF-1alpha, a VEGF regulator, occurred
Beclin-1↓, GNL also decreases autophagy through downregulation of BNIP3 and beclin-1 expression, which increases apoptotic cell death through HIF-1α signaling.

4353- MF,  Chemo,    Pulsed Electromagnetic Field Enhances Doxorubicin-induced Reduction in the Viability of MCF-7 Breast Cancer Cells
- in-vitro, BC, MCF7
TumCCA↑, PEMF enhances the anticancer activity in DOX-treated MCF-7 breast cancer cells by increasing G1 cell cycle arrest and caspase-dependent apoptosis.
Apoptosis↑, we report that PEMF stimulation enhances the reduction in the cell viability by enhancing cell cycle arrest and apoptosis in MCF-7 breast cancer cells.
eff↑, extremely low frequency (ELF)-EMF can increase the cytotoxic effect of DOX on MCF-7 breast cancer cells compared with treatment with DOX alone
TumCCA↑, we report here that PEMF enhances DOX-induced cell cycle arrest in G1 phase and caspase-dependent apoptosis
Casp↝, PEMF promoted the DOX-induced activation of caspases-8, -9, and -7
p‑CDK2↓, combined treatment with DOX and PEMF produced the further reduction in CDK2 phosphorylation and cyclin E2 expression when compared to treatment with DOX alone
cycE/CCNE↓,
Fas↑, expression of Fas and Bax was elevated to a larger degree in the DOX/PEMF-treated cells than in the DOX-treated cells
BAX↑,
survivin↓, expression of survivin was decreased in the DOX-treated cells and further reduced in the DOX/PEMF-treated cells
Mcl-1↓, Mcl-1 expression was reduced in the DOX/PEMF-treated cells compared to the DOX-treated cells
cl‑PARP↑, increased PARP cleavage was observed in the DOX/PEMF-treated cells
cl‑Casp7↑, caspase-7 was higher in the DOX-treated cells than in the control group and was further higher in the DOX/PEMF-treated cells
cl‑Casp8↑, Cleavage of caspase-8 and -9 were elevated in the DOX-treated cells and increased even more in the DOX/PEMF-treated cells
cl‑Casp9↑,


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(tgid=1) ⓘ

ROS↓, 1,  

Cell Death(tgid=5) ⓘ

Apoptosis↑, 3,   BAX↑, 1,   Casp↝, 3,   cl‑Casp7↑, 1,   cl‑Casp8↑, 1,   cl‑Casp9↑, 1,   Fas↑, 1,   Mcl-1↓, 1,   survivin↓, 1,  

Transcription & Epigenetics(tgid=7) ⓘ

miR-21↝, 1,  

Autophagy & Lysosomes(tgid=9) ⓘ

Beclin-1↓, 1,  

DNA Damage & Repair(tgid=10) ⓘ

P53↝, 1,   PARP↝, 1,   cl‑PARP↑, 1,  

Cell Cycle & Senescence(tgid=11) ⓘ

p‑CDK2↓, 1,   cycE/CCNE↓, 1,   TumCCA↑, 3,  

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

STAT3↓, 1,   TumCG↑, 1,  

Migration(tgid=13) ⓘ

MMPs↝, 1,   TumCMig↓, 1,   TumCP↓, 2,   TumMeta↓, 1,  

Angiogenesis & Vasculature(tgid=14) ⓘ

angioG↓, 1,   Hif1a↓, 1,   VEGF↝, 1,  

Immune & Inflammatory Signaling(tgid=16) ⓘ

NF-kB↝, 1,  

Drug Metabolism & Resistance(tgid=21) ⓘ

eff↑, 1,   selectivity↑, 1,  
Total Targets: 30

Pathway results for Effect on Normal Cells:


NA, unassigned(tgid=0) ⓘ

AntiBio↑, 1,  

Redox & Oxidative Stress(tgid=1) ⓘ

antiOx↑, 1,   Catalase↑, 1,   GPx↑, 1,   GSH↑, 1,   GSTs↑, 1,   HO-1↑, 1,   NRF2↑, 1,   SOD↑, 1,   TBARS↓, 1,  

Cell Death(tgid=5) ⓘ

iNOS↓, 1,   survivin↓, 1,  

Angiogenesis & Vasculature(tgid=14) ⓘ

NO↓, 1,  

Immune & Inflammatory Signaling(tgid=16) ⓘ

COX2↓, 1,   IL1β↓, 1,   Inflam↓, 1,   NF-kB↓, 1,  

Synaptic & Neurotransmission(tgid=18) ⓘ

AChE↓, 1,  

Protein Aggregation(tgid=19) ⓘ

XO↓, 1,  

Functional Outcomes(tgid=23) ⓘ

AntiCan↑, 1,   memory↑, 1,   neuroP↑, 1,  
Total Targets: 22

Scientific Paper Hit Count for: Casp, caspase
1 Garcinol
1 Gemcitabine (Gemzar)
1 Geraniol
1 Magnetic Fields
1 Chemotherapy
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

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