DFF45 Cancer Research Results

DFF45, DNA Fragmentation Factor 45 Gene: Click to Expand ⟱
Source:
Type:
DFF45 was expressed preferably in low-stage neuroblastoma tumors, and to a lesser degree in high-stage neuroblastomas.
Scientific Papers found: Click to Expand⟱
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↓,

821- GAR,    Garcinol inhibits cell growth in hepatocellular carcinoma Hep3B cells through induction of ROS-dependent apoptosis
- in-vitro, Liver, Hep3B
ROS↑, Garcinol treatment led to the accumulation of reactive oxygen species (ROS)
CHOP↑, increased GADD153 expression
MMP↓,
Bax:Bcl2↑,
Casp8↑,
Casp3↑, 13x
Casp9↑, 7.8x
cl‑PARP↑,
DFF45↑,

48- QC,    Quercetin Potentiates Apoptosis by Inhibiting Nuclear Factor-kappaB Signaling in H460 Lung Cancer Cells
- in-vitro, NSCLC, H460
TRAILR↑, quercetin increased the expression of genes associated with death receptor signaling tumor necrosis factor-related apoptosis-inducing ligand receptor (TRAILR), caspase-10, interleukin (IL) 1R DNA fragmentation faotor 45 (DFF45), tumor necrosis fact
Casp10↑,
DFF45↑,
TNFR 1↑,
Fas↑,
NF-kB↓, Quercetin Potentiates Apoptosis by Inhibiting Nuclear Factor-kappaB Signaling in H460 Lung Cancer Cells
IKKα↓,

923- QC,    Quercetin as an innovative therapeutic tool for cancer chemoprevention: Molecular mechanisms and implications in human health
- Review, Var, NA
ROS↑, decided by the availability of intracellular reduced glutathione (GSH),
GSH↓, extended exposure with high concentration of quercetin causes a substantial decline in GSH levels
Ca+2↝,
MMP↓,
Casp3↑, activation of caspase-3, -8, and -9
Casp8↑,
Casp9↑,
other↓, when p53 is inhibited, cancer cells become vulnerable to quercetin-induced apoptosis
*ROS↓, Quercetin (QC), a plant-derived bioflavonoid, is known for its ROS scavenging properties and was recently discovered to have various antitumor properties in a variety of solid tumors.
*NRF2↑, Moreover, the therapeutic efficacy of QC has also been defined in rat models through the activation of Nrf-2/HO-1 against high glucose-induced damage
HO-1↑,
TumCCA↑, QC increases cell cycle arrest via regulating p21WAF1, cyclin B, and p27KIP1
Inflam↓, QC-mediated anti-inflammatory and anti-apoptotic properties play a key role in cancer prevention by modulating the TLR-2 (toll-like receptor-2) and JAK-2/STAT-3 pathways and significantly inhibit STAT-3 tyrosine phosphorylation within inflammatory ce
STAT3↓,
DR5↑, several studies showed that QC upregulated the death receptor (DR)
P450↓, it hinders the activity of cytochrome P450 (CYP) enzymes in hepatocytes
MMPs↓, QC has also been shown to suppress metastatic protein expression such as MMPs (matrix metalloproteases)
IFN-γ↓, QC is its ability to inhibit inflammatory mediators including IFN-γ, IL-6, COX-2, IL-8, iNOS, TNF-α,
IL6↓,
COX2↓,
IL8↓,
iNOS↓,
TNF-α↓,
cl‑PARP↑, Induced caspase-8, caspase-9, and caspase-3 activation, PARP cleavage, mitochondrial membrane depolarization,
Apoptosis↑, increased apoptosis and p53 expression
P53↑,
Sp1/3/4↓, HT-29 colon cancer cells: decreased the expression of Sp1, Sp3, Sp4 mrna, and survivin,
survivin↓,
TRAILR↑, H460 Increased the expression of TRAILR, caspase-10, DFF45, TNFR 1, FAS, and decreased the expression of NF-κb, ikkα
Casp10↑,
DFF45↑,
TNFR 1↑,
Fas↑,
NF-kB↓,
IKKα↓,
cycD1/CCND1↓, SKOV3 Reduction in cyclin D1 level
Bcl-2↓, MCF-7, HCC1937, SK-Br3, 4T1, MDA-MB-231 Decreased Bcl-2 expression, increasedBax expression, inhibition of PI3K-Akt pathway
BAX↑,
PI3K↓,
Akt↓,
E-cadherin↓, MDA-MB-231 Induced the expression of E-cadherin and downregulated vimentin levels, modulation of β-catenin target genes such as cyclin D1 and c-Myc
Vim↓,
β-catenin/ZEB1↓,
cMyc↓,
EMT↓, MCF-7 Suppressed the epithelial–mesenchymal transition process, upregulated E-cadherin expression, downregulated vimentin and MMP-2 expression, decreased Notch1 expression
MMP2↓,
NOTCH1↓,
MMP7↓, PANC-1, PATU-8988 Decreased the secretion of MMP and MMP7, blocked the STAT3 signaling pathway
angioG↓, PC-3, HUVECs Reduced angiogenesis, increased TSP-1 protein and mrna expression
TSP-1↑,
CSCs↓, PC-3 and LNCaP cells Activated capase-3/7 and inhibit the expression of Bcl-2, surviving and XIAP in CSCs.
XIAP↓,
Snail↓, inhibiting the expression of vimentin, slug, snail and nuclear β-catenin, and the activity of LEF-1/TCF responsive reporter
Slug↓,
LEF1↓,
P-gp↓, MCF-7 and MCF-7/dox cell lines Downregulation of P-gp expression
EGFR↓, MCF-7 and MDA-MB-231 cells Suppressed EGFR signaling and inhibited PI3K/Akt/mTOR/GSK-3β
GSK‐3β↓,
mTOR↓,
RAGE↓, IA Paca-2, BxPC3, AsPC-1, HPAC and PANC1 Silencing RAGE expression
HSP27↓, Breast cancer In vivo NOD/SCID mice Inhibited the overexpression of Hsp27
VEGF↓, QC significantly reversed an elevation in profibrotic markers (VEGF, IL-6, TGF, COL-1, and COL-3)
TGF-β↓,
COL1↓,
COL3A1↓,


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 ⓘ

GSH↓, 1,   HO-1↑, 1,   ROS↑, 3,  

Mitochondria & Bioenergetics ⓘ

MMP↓, 2,   MPT↑, 1,   XIAP↓, 1,  

Core Metabolism/Glycolysis ⓘ

cMyc↓, 1,  

Cell Death ⓘ

Akt↓, 2,   Apoptosis↑, 2,   BAX↑, 1,   Bax:Bcl2↑, 1,   Bcl-2↓, 1,   Casp10↑, 2,   Casp3↑, 3,   Casp6↑, 1,   Casp8↑, 2,   Casp9↑, 2,   Cyt‑c↑, 1,   DR5↑, 1,   Fas↑, 2,   iNOS↓, 1,   survivin↓, 1,   TNFR 1↑, 2,   TRAILR↑, 2,  

Kinase & Signal Transduction ⓘ

Sp1/3/4↓, 1,  

Transcription & Epigenetics ⓘ

other↓, 1,   tumCV↓, 1,  

Protein Folding & ER Stress ⓘ

CHOP↑, 1,   HSP27↓, 1,  

Autophagy & Lysosomes ⓘ

TumAuto↑, 1,  

DNA Damage & Repair ⓘ

DFF45↑, 4,   DNMT1↓, 1,   DNMT3A↓, 1,   P53↑, 1,   PARP↑, 1,   cl‑PARP↑, 2,  

Cell Cycle & Senescence ⓘ

cycD1/CCND1↓, 1,   TumCCA↑, 2,  

Proliferation, Differentiation & Cell State ⓘ

CSCs↓, 1,   EMT↓, 2,   FOXO3↓, 1,   GSK‐3β↓, 1,   mTOR↓, 1,   mTORC2↓, 1,   NOTCH1↓, 1,   PI3K↓, 2,   STAT3↓, 1,  

Migration ⓘ

5LO↓, 1,   Ca+2↝, 1,   COL1↓, 1,   COL3A1↓, 1,   E-cadherin↓, 1,   E-cadherin↑, 1,   LEF1↓, 1,   MMP2↓, 1,   MMP7↓, 1,   MMPs↓, 1,   RAGE↓, 1,   Slug↓, 1,   Snail↓, 2,   TGF-β↓, 1,   TSP-1↑, 1,   TumMeta↓, 1,   Vim↓, 2,   β-catenin/ZEB1↓, 1,  

Angiogenesis & Vasculature ⓘ

angioG↓, 2,   EGFR↓, 1,   VEGF↓, 1,  

Barriers & Transport ⓘ

P-gp↓, 1,  

Immune & Inflammatory Signaling ⓘ

COX2↓, 2,   IFN-γ↓, 1,   IKKα↓, 2,   IL6↓, 1,   IL8↓, 1,   Inflam↓, 1,   NF-kB↓, 3,   TNF-α↓, 1,  

Drug Metabolism & Resistance ⓘ

ChemoSen↑, 1,   P450↓, 1,   RadioS↑, 1,  

Clinical Biomarkers ⓘ

EGFR↓, 1,   IL6↓, 1,   RAGE↓, 1,  
Total Targets: 83

Pathway results for Effect on Normal Cells:


Redox & Oxidative Stress ⓘ

NRF2↑, 1,   ROS↓, 2,  
Total Targets: 2

Scientific Paper Hit Count for: DFF45, DNA Fragmentation Factor 45 Gene
2 Quercetin
1 Eugenol
1 Garcinol
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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