KDR/FLK-1 Cancer Research Results
KDR/FLK-1, Kinase insert Domain-Containing Receptor/Fetal Liver Kinase-1: Click to Expand ⟱
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| Type: receptor tyrosine kinase |
KDR/FLK-1 (Kinase insert Domain-Containing Receptor/Fetal Liver Kinase-1) is a receptor tyrosine kinase that plays a crucial role in angiogenesis, the process of new blood vessel formation.
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Scientific Papers found: Click to Expand⟱
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vitro+vivo, |
Ovarian, |
HO-8910 |
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vitro+vivo, |
Nor, |
HUVECs |
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angioG↓, 0.5 approximately 50 micromol/l
TumCG↓,
VEGF↓, remarkably lowered VEGF expression on tumor cells
KDR/FLK-1↓,
*toxicity↓, known low toxicity of ART
IL6↓,
IL1↓, IL-1β
TNF-α↓,
TGF-β↓, TGF-β1
NF-kB↓,
MIP2↓,
PGE2↓,
NO↓,
Hif1a↓,
KDR/FLK-1↓,
VEGF↓,
MMP2↓,
TIMP2↑,
ITGB1↑,
NCAM↑,
p‑ATM↑,
p‑ATR↑,
p‑CHK1↑,
p‑Chk2↑,
Wnt/(β-catenin)↓,
PI3K↓,
Akt↓,
ERK↓, ERK1/2
cMyc↓,
mTOR↓,
survivin↓,
cMET↓,
EGFR↓,
cycD1/CCND1↓,
cycE1↓,
CDK4/6↓,
p16↑,
p27↑,
Apoptosis↑,
TumAuto↑,
Ferroptosis↑,
oncosis↑,
TumCCA↑, G0/G1 into M phase, G0/G1 into S phase, G1 and G2/M
ROS↑, ovarian cancer cell line model, artesunate induced oxidative stress, DNA double-strand breaks (DSBs) and downregulation of RAD51 foci
DNAdam↑,
RAD51↓,
HR↓,
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in-vitro, |
Melanoma, |
RPMI-8226 |
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IGF-1↓, Shikonin Induces Apoptosis by Inhibiting Phosphorylation of IGF-1 Receptor in Myeloma Cells
Apoptosis↑, Shikonin suppressed the cellular growth of RPMI8226 and IM9 myeloma cells, via induction of apoptosis in a dose (0–1 μM)- and time (0–24 h)-dependent manner.
TumCCA↑, Treatment with 0.5 μM Shikonin rapidly increased the population of cells in the G0/G1 phase with reduction of cells in the S phase
MMP↓, Shikonin-induced apoptosis was in association with the loss of mitochondrial transmembrane potentials, and activation of caspase-3.
Casp3↑,
P53↑, Expression of p53 and Bax proteins was increased with down-regulation of Mcl-1 protein
BAX↑,
Mcl-1↓,
EGFR↓, Shikonin has reported to be an inhibitor of protein tyrosine kinase such as EGFR, v-Src, and KDR/Flk-1.
Src↑,
KDR/FLK-1↓,
p‑IGF-1↓, Shikonin inhibited phosphorylation of IGF-1 receptor as early as 30 min with inhibition of PI3K/Akt signaling
PI3K↓,
Akt↓,
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 ⓘ
Ferroptosis↑, 1, ROS↑, 1,
Mitochondria & Bioenergetics ⓘ
MMP↓, 1,
Core Metabolism/Glycolysis ⓘ
cMyc↓, 1,
Cell Death ⓘ
Akt↓, 2, Apoptosis↑, 2, BAX↑, 1, Casp3↑, 1, p‑Chk2↑, 1, Ferroptosis↑, 1, Mcl-1↓, 1, oncosis↑, 1, p27↑, 1, survivin↓, 1,
Autophagy & Lysosomes ⓘ
TumAuto↑, 1,
DNA Damage & Repair ⓘ
p‑ATM↑, 1, p‑ATR↑, 1, p‑CHK1↑, 1, DNAdam↑, 1, HR↓, 1, p16↑, 1, P53↑, 1, RAD51↓, 1,
Cell Cycle & Senescence ⓘ
cycD1/CCND1↓, 1, cycE1↓, 1, TumCCA↑, 2,
Proliferation, Differentiation & Cell State ⓘ
cMET↓, 1, ERK↓, 1, IGF-1↓, 1, p‑IGF-1↓, 1, mTOR↓, 1, PI3K↓, 2, Src↑, 1, TumCG↓, 1, Wnt/(β-catenin)↓, 1,
Migration ⓘ
CDK4/6↓, 1, ITGB1↑, 1, MMP2↓, 1, NCAM↑, 1, TGF-β↓, 1, TIMP2↑, 1,
Angiogenesis & Vasculature ⓘ
angioG↓, 1, EGFR↓, 2, Hif1a↓, 1, KDR/FLK-1↓, 3, NO↓, 1, VEGF↓, 2,
Immune & Inflammatory Signaling ⓘ
IL1↓, 1, IL6↓, 1, MIP2↓, 1, NF-kB↓, 1, PGE2↓, 1, TNF-α↓, 1,
Clinical Biomarkers ⓘ
EGFR↓, 2, IL6↓, 1,
Total Targets: 55
Pathway results for Effect on Normal Cells:
Functional Outcomes ⓘ
toxicity↓, 1,
Total Targets: 1
Scientific Paper Hit Count for: KDR/FLK-1, Kinase insert Domain-Containing Receptor/Fetal Liver Kinase-1
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#:789 State#:% Dir#:1
wNotes=on sortOrder:rid,rpid
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