Casp6 Cancer Research Results

Casp6, Caspase-6: Click to Expand ⟱
Source:
Type:
A member of the caspase family, a group of cysteine proteases that play a crucial role in programmed cell death, also known as apoptosis.
Caspase-6 has been found to be overexpressed in various types of cancer, including breast, lung, and colon cancer. However, its expression levels and activity can vary depending on the type of cancer and the stage of disease progression.
Inhibitors of caspase-6 have been shown to have anti-tumor effects in preclinical studies, while activators of caspase-6 have been found to induce apoptosis in cancer cells.
Scientific Papers found: Click to Expand⟱
324- AgNPs,  CPT,    Silver Nanoparticles Potentiates Cytotoxicity and Apoptotic Potential of Camptothecin in Human Cervical Cancer Cells
- in-vitro, Cerv, HeLa
ROS↑,
Casp3↑,
Casp9↑,
Casp6↑,
GSH↓,
SOD↓,
GPx↓,
MMP↓, loss of
P53↑,
P21↑,
Cyt‑c↑,
BID↑,
BAX↑,
Bcl-2↓,
Bcl-xL↓,
Akt↓,
Raf↓,
ERK↓,
MAP2K1/MEK1↓,
JNK↑,
p38↑,

5897- CAR,    Carvacrol Selectively Induces Mitochondria-Related Apoptotic Signaling in Primary Breast Cancer-Associated Fibroblasts
- in-vitro, BC, NA
Bax:Bcl2↑, marked increase in the BAX/BCL-XL ratio
PPARα↓, carvacrol reduced PPARα expression and NF-κB nuclear localization, increased SIRT1 and SIRT3 levels, selectively suppressed MMP-3
NF-kB↓,
SIRT1↑,
SIRT3↑,
MMP3↓,
selectivity↑, Carvacrol selectively targets breast cancer-associated fibroblasts by inducing mitochondria-related apoptotic signaling while largely sparing normal fibroblasts.
Bcl-2↓, In breast cancer lines, CV has been reported to down-regulate Bcl-2, up-regulate Bax, and induce caspase-3/-6/-9 activation in a dose-dependent manner, consistent with mitochondrial apoptosis
BAX↑,
Casp3↑,
Casp6↑,
Casp9↑,
mt-Apoptosis↑,

6390- Eug,    Molecular mechanisms of eugenol as an antitumour bioactive compound: A comprehensive review
- Review, Var, NA
TumCCA↑, Eugenol via two pathways; intrinsic and extrinsic can induce apoptosis, cause cell cycle arrest together with its antioxidant/antiinflammatory effects against angiogenesis and metastasis.
angioG↓,
TumMeta↓,
tumCV↓, eugenol reduced cell viability in a dose-dependent manner
Casp3↑, enhancement of caspase-3/6 and cleavage of caspase substrates including DFF45, PARP, and lamin A
Casp6↑,
DFF45↑,
PARP↑,
ROS↑, apoptosis initiated by eugenol in human promyelocytic leukaemia cells was evidenced to be mediated via induction of reactive oxygen species (ROS) generation and the release of cytochrome c through mitochondrial permeability transition
Cyt‑c↑,
MPT↑,
*ROS↓, Eugenol also shows high antioxidant activity involved in scavenging free radicals to decrease oxidative stress, a crucial factor in carcinogenesis. It acts as an antioxidant and pro-oxidant, depending on the conditions in a cell.
NF-kB↓, Eugenol has been demonstrated to have anti-inflammatory activities by downregulating NF-κB signalling pathway
COX2↓, Eugenol has been shown to inhibit COX-2 expression and activity, thereby exerting its anti-inflammatory and anti-tumour effects
5LO↓, eugenol has the potential to bind to both COX-2 and 5-lipoxygenase (5-LOX) enzymes, indicating its role as an anti-inflammatory compound.
EMT↓, eugenol can suppress EMT in various cancer models.
Snail↓, inhibition of EMT by downregulating the expression of Snail, a key transcription factor that represses E-cadherin expression, while simultaneously increasing E-cadherin expression
E-cadherin↑,
Vim↓, reducing vimentin expression
PI3K↓, eugenol might inhibit the PI3K/ Akt/ mTOR pathway in different cancer cell lines.
Akt↓,
mTORC2↓,
TumAuto↑, eugenol induced autophagy and apoptosis in breast cells by inhibiting the PI3K/AKT/FOXO3a pathway
FOXO3↓,
Apoptosis↑,
ChemoSen↑, Eugenol has shown promising adjuvant efficacy in cancer therapies, with evidence of synergistic effects with conventional chemotherapeutics, natural products and radiation therapy
RadioS↑,
DNMT1↓, downregulates the expression of DNA methyltransferases DNMT1 and DNMT3A in the breast cancer-associated fibroblasts (CAFs)
DNMT3A↓,

4519- MAG,    Magnolol: A Neolignan from the Magnolia Family for the Prevention and Treatment of Cancer
- Review, Var, NA
*antiOx↑, anti-oxidant [70], anti-inflammatory [71], anti-bacterial [10], anti-thrombotic or anti-platelet
*Inflam↓,
*Bacteria↓,
*AntiAg↑,
*BBB↑, MAG can easily cross the blood brain barrier
*BioAv↓, bioavailability is in the region of 10%
BAD↑, MAG increased the expression of Bad, Bcl-XS, caspases-3, -6, and -9 and c-Jun N-terminal kinases (JNK) and suppressed the expression of Bcl-xL
Casp3↑,
Casp6↑,
Casp9↑,
JNK↑,
Bcl-xL↓,
PTEN↑, MAG also induced apoptosis by enhancing the expression of PTEN and down-regulation of AKT
Akt↓,
NF-kB↓, MAG induces cell death and reduces cell proliferation by inhibition of NF-κB activity
MMP7↓, MAG inhibits cancer metastasis by reducing the expression of matrix metalloproteinase-7, -9 (MMP-7, -9) and urokinase plasminogen activator (uPA)
MMP9↓,
uPA↓,
Hif1a↓, MAG attenuated angiogenesis in vitro and in vivo which is mediated by inhibition of the expression of hypoxia-inducible factors-1α (HIF-1α) and vascular endothelial growth factor (VEGF) secretion in human bladder cancer cells
VEGF↓,
FOXO3↓, MAG downregulated the expression of transcriptional factor Forkhead box O3 (FoxO3), ubiquitin ligase, MuRF-1 and MAFbx/atrogin-1.
Ca+2↑, ↑Cytosolic free Ca (2+);
TumCCA↑, ↑Cell cycle arrest at G2/M phase, ROS, release of cyt-c,
ROS↑,
Cyt‑c↑,


Showing Research Papers: 1 to 4 of 4

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 4

Pathway results for Effect on Cancer / Diseased Cells:


Redox & Oxidative Stress ⓘ

GPx↓, 1,   GSH↓, 1,   ROS↑, 3,   SIRT3↑, 1,   SOD↓, 1,  

Mitochondria & Bioenergetics ⓘ

MMP↓, 1,   MPT↑, 1,   Raf↓, 1,  

Core Metabolism/Glycolysis ⓘ

PPARα↓, 1,   SIRT1↑, 1,  

Cell Death ⓘ

Akt↓, 3,   Apoptosis↑, 1,   mt-Apoptosis↑, 1,   BAD↑, 1,   BAX↑, 2,   Bax:Bcl2↑, 1,   Bcl-2↓, 2,   Bcl-xL↓, 2,   BID↑, 1,   Casp3↑, 4,   Casp6↑, 4,   Casp9↑, 3,   Cyt‑c↑, 3,   JNK↑, 2,   p38↑, 1,  

Transcription & Epigenetics ⓘ

tumCV↓, 1,  

Autophagy & Lysosomes ⓘ

TumAuto↑, 1,  

DNA Damage & Repair ⓘ

DFF45↑, 1,   DNMT1↓, 1,   DNMT3A↓, 1,   P53↑, 1,   PARP↑, 1,  

Cell Cycle & Senescence ⓘ

P21↑, 1,   TumCCA↑, 2,  

Proliferation, Differentiation & Cell State ⓘ

EMT↓, 1,   ERK↓, 1,   FOXO3↓, 2,   MAP2K1/MEK1↓, 1,   mTORC2↓, 1,   PI3K↓, 1,   PTEN↑, 1,  

Migration ⓘ

5LO↓, 1,   Ca+2↑, 1,   E-cadherin↑, 1,   MMP3↓, 1,   MMP7↓, 1,   MMP9↓, 1,   Snail↓, 1,   TumMeta↓, 1,   uPA↓, 1,   Vim↓, 1,  

Angiogenesis & Vasculature ⓘ

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

Immune & Inflammatory Signaling ⓘ

COX2↓, 1,   NF-kB↓, 3,  

Drug Metabolism & Resistance ⓘ

ChemoSen↑, 1,   RadioS↑, 1,   selectivity↑, 1,  
Total Targets: 59

Pathway results for Effect on Normal Cells:


Redox & Oxidative Stress ⓘ

antiOx↑, 1,   ROS↓, 1,  

Migration ⓘ

AntiAg↑, 1,  

Barriers & Transport ⓘ

BBB↑, 1,  

Immune & Inflammatory Signaling ⓘ

Inflam↓, 1,  

Drug Metabolism & Resistance ⓘ

BioAv↓, 1,  

Infection & Microbiome ⓘ

Bacteria↓, 1,  
Total Targets: 7

Scientific Paper Hit Count for: Casp6, Caspase-6
1 Silver-NanoParticles
1 Camptothecin
1 Carvacrol
1 Eugenol
1 Magnolol
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#:620  State#:%  Dir#:2
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