SCF Cancer Research Results
SCF, Stem Cell Factor: Click to Expand ⟱
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Important role in hematopoiesis (formation of blood cells), spermatogenesis, and melanogenesis. A cytokine that specifically binds the tyrosine kinase receptor c-KIT.
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Scientific Papers found: Click to Expand⟱
TumCP↓, chrysin has shown to inhibit proliferation and induce apoptosis, and is more potent than other tested flavonoids in leukemia cells
Apoptosis↑,
Casp↑, chrysin is likely to act via activation of caspases and inactivation of Akt signaling in the cells.
PCNA↓, inhibited the growth of cervical cancer cells, HeLa, via apoptosis induction and down-regulated the proliferating cell nuclear antigen (PCNA) in the cells.
p38↑, chrysin potentially induced p38, therefore activated NFkappaB/p65 in the HeLa cells
NF-kB↑,
DNAdam↑, only apigenin, chrysin, quercetin, galangin, luteolin and fisetin were found to clearly induce the oligonucleosomal DNA fragmentation at 50 μM after 6 h of treatment
XIAP↓, down-regulation of X-linked inhibitor of apoptosis protein (XIAP) in the U937 cells
Cyt‑c↑, (1) chrysin mediated the release of cytochrome c from mitochondria into the cytoplasm;
Casp3↑, (2) chrysin induced elevated caspase-3 activity and proteolytic cleavage of its downstream targets, such as phospholipase C-gamma-1 (PLC-gamma1), which is correlated with down-regulation of XIAP;
Akt↓, (3) chrysin decreased phosphorylated Akt levels in cells where the PI3K pathway plays a role in regulating the mechanism.
SCF↓, Chrysin has also been reported to have the ability to abolish the stem cell factor (SCF)/c-Kit signaling by inhibiting the PI3K pathway
hTERT/TERT↓, A significant decrease in human telomerase reverse transcriptase (hTERT) expression levels was also observed in leukemia cells treated with 60 ng/mL Manisa propolis, owing to its constituent of chrysin
COX2↓, Chrysin also inhibited the lipopolysaccharide-induced COX-2 expression via inhibition of nuclear factor IL-6 (NF-IL6)
*Inflam↓, anti-inflammatory [21] and anti-oxidant effects [22], and has shown cancer chemopreventive activity via induction of apoptosis in diverse range of human and rat cell types.
*antiOx↑,
*chemoPv↑,
AR-V7?,
CYP19?, Chrysin has recently shown to be a potent inhibitor of aromatase [18] and of human immunodeficiency virus activation in models of latent infection
Apoptosis↑, chrysin inhibits cancer growth through induction of apoptosis, alteration of cell cycle and inhibition of angiogenesis, invasion and metastasis without causing any toxicity and undesirable side effects to normal cells
TumCCA↑,
angioG↓,
TumCI↓,
TumMeta↑,
*toxicity↓,
selectivity↑,
chemoPv↑, Induction of phase II detoxification enzymes, such as glutathione S-transferase (GST) or NAD(P)H:quinone oxidoreductase (QR) is one of the major mechanism of protection against initiation of carcinogenesis
*GSTs↑,
*NADPH↑,
*GSH↑, upregulation of antioxidant and carcinogen detoxification enzymes (glutathione (GSH), glutathione peroxidase (GPx), glutathione reductase (GR), GST and QR)
HDAC8↓, inhibits of HDAC8 enzymatic activity
Hif1a↓, Prostate DU145: Inhibits HIF-1a expression through Akt signaling and abrogation of VEGF expression
*ROS↓, chrysin (20 and 40 mg/kg) was shown to exhibit chemopreventive activity by ameliorating oxidative stress and
inflammation via NF-kB pathway
*NF-kB↓,
SCF↓, Chrysin has also been reported to have the ability to abolish the stem cell factor (SCF)/c-Kit signaling in human myeloid leukemia cells by preventing the PI3 K pathway
cl‑PARP↑, (PARP) and caspase-3 and concurrently decreasing pro-survival proteins survivin and XIAP
survivin↓,
XIAP↓,
Casp3↑, activation of caspase-3 and -9.
Casp9↑,
GSH↓, chrysin sustains a significant depletion of intracellular GSH concentrations in human NSCLC cells
ChemoSen↑, chrysin potentiates cisplatin toxicity, in part, via synergizing pro-oxidant effects of cisplatin by inducing mitochondrial dysfunction, and by depleting cellular GSH, an important antioxidant defense
Fenton↑, ability to participate in a fenton type chemical reaction
P21↑, upregulation of p21 independent of p53 status and decrease in cyclin D1, CDK2 protein levels
P53↑,
cycD1/CCND1↓,
CDK2↓,
STAT3↓, chrysin inhibits angiogenesis through inhibition of STAT3 and VEGF release mediated by hypoxia through Akt signaling pathway
VEGF↓,
Akt↓,
NRF2↓, Chrysin treatment significantly reduced
nrf2 expression in cells at both the mRNA and protein levels
through down-regulation of PI3K-Akt and ERK pathways.
BAD↓,
cl‑PARP↑,
Casp7↑,
IκB↓,
Ki-67↓,
VEGF↓,
EGFR↓,
FGF↓,
TGF-β↓,
TNF-α↓,
SCF↓,
Bax:Bcl2↑,
NF-kB↓,
chemoP↑, This study provides a novel regimen to enhance the therapeutic effect of Doc in a less-toxic manner and reduce its risk of side effects in treatment of CRPC.
ChemoSen↑, GT and Q with LD Doc significantly enhanced the potency of Doc 2-fold and reduced tumor growth by 62 % compared to LD Doc in 7-weeks intervention.
TumVol↓,
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 ⓘ
Fenton↑, 1, GSH↓, 1, NRF2↓, 1,
Mitochondria & Bioenergetics ⓘ
XIAP↓, 2,
Cell Death ⓘ
Akt↓, 2, Apoptosis↑, 2, BAD↓, 1, Bax:Bcl2↑, 1, Casp↑, 1, Casp3↑, 2, Casp7↑, 1, Casp9↑, 1, Cyt‑c↑, 1, hTERT/TERT↓, 1, p38↑, 1, survivin↓, 1,
DNA Damage & Repair ⓘ
DNAdam↑, 1, P53↑, 1, cl‑PARP↑, 2, PCNA↓, 1,
Cell Cycle & Senescence ⓘ
CDK2↓, 1, cycD1/CCND1↓, 1, P21↑, 1, TumCCA↑, 1,
Proliferation, Differentiation & Cell State ⓘ
AR-V7?, 1, FGF↓, 1, HDAC8↓, 1, SCF↓, 3, STAT3↓, 1,
Migration ⓘ
Ki-67↓, 1, TGF-β↓, 1, TumCI↓, 1, TumCP↓, 1, TumMeta↑, 1,
Angiogenesis & Vasculature ⓘ
angioG↓, 1, EGFR↓, 1, Hif1a↓, 1, VEGF↓, 2,
Immune & Inflammatory Signaling ⓘ
COX2↓, 1, IκB↓, 1, NF-kB↓, 1, NF-kB↑, 1, TNF-α↓, 1,
Hormonal & Nuclear Receptors ⓘ
CYP19?, 1,
Drug Metabolism & Resistance ⓘ
ChemoSen↑, 2, selectivity↑, 1,
Clinical Biomarkers ⓘ
EGFR↓, 1, hTERT/TERT↓, 1, Ki-67↓, 1,
Functional Outcomes ⓘ
chemoP↑, 1, chemoPv↑, 1, TumVol↓, 1,
Total Targets: 52
Pathway results for Effect on Normal Cells:
Redox & Oxidative Stress ⓘ
antiOx↑, 1, GSH↑, 1, GSTs↑, 1, ROS↓, 1,
Core Metabolism/Glycolysis ⓘ
NADPH↑, 1,
Immune & Inflammatory Signaling ⓘ
Inflam↓, 1, NF-kB↓, 1,
Functional Outcomes ⓘ
chemoPv↑, 1, toxicity↓, 1,
Total Targets: 9
Scientific Paper Hit Count for: SCF, Stem Cell Factor
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#:436 State#:% Dir#:1
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