CDK2 Cancer Research Results
CDK2, Cyclin-dependent kinase 2: Click to Expand ⟱
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| Type: |
(CDK2) complex is significantly over-activated in many cancers.
CDK2 (Cyclin-Dependent Kinase 2) is a serine/threonine kinase that regulates late G1 and S phase of the cell cycle.
CDK2 interacts with and phosphorylates proteins in pathways such as DNA damage, intracellular transport, protein degradation, signal transduction, DNA and RNA metabolism and translation.
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Scientific Papers found: Click to Expand⟱
TumCP↓, reported inhibitory effects on cancer cell proliferation, invasion and migration.
TumCI↓,
TumCMig↓,
Apoptosis↑, ART has been reported to induce apoptosis, differentiation and autophagy in colorectal cancer cells by impairing angiogenesis
Diff↑,
TumAuto↑,
angioG↓,
TumCCA↑, inducing cell cycle arrest (11), upregulating ROS levels, regulating signal transduction [for example, activating the AMPK-mTOR-Unc-51-like autophagy activating kinase (ULK1) pathway in human bladder cancer cells]
ROS↑,
AMPK↑,
mTOR↑,
ChemoSen↑, ART has been shown to restore the sensitivity of a number of cancer types to chemotherapeutic drugs by modulating various signaling pathways
Tf↑, ART could upregulate the mRNA levels of transferrin receptor (a positive regulator of ferroptosis), thus inducing apoptosis and ferroptosis in A549 non-small cell lung cancer (NSCLC) cells.
Ferroptosis↑,
Ferritin↓, ferritin degradation, lipid peroxidation and ferroptosis
lipid-P↑,
CDK1↑, Cyclin-dependent kinase 1, 2, 4 and 6
CDK2↑,
CDK4↑,
CDK6↑,
SIRT1↑, Sirt1 levels
COX2↓,
IL1β↓, IL-1? ?
survivin↓, ART can selectively downregulate the expression of survivin and induce the DNA damage response in glial cells to increase cell apoptosis and cell cycle arrest, resulting in increased sensitivity to radiotherapy
DNAdam↑,
RadioS↑,
AntiCan↑, Studies have shown its anti-tumor effect in gastric cancer, liver cancer, pancreatic cancer, breast cancer, colorectal cancer, lung cancer and other malignant tumors
Apoptosis↑,
TumCP↓,
TumMeta↓,
TumCI↓,
TumAuto↑,
VEGFR2↓, inhibition of VEGFR-2 signaling
MAPK↓, MAPK and PI3K/Akt pathways
PI3K↓,
Akt↓,
PD-1↓, Downregulation of VEGFR-2 and PD-1 expression
NOTCH↓, Inhibition of Akt and Notch
PCNA↓, regulation of the expression of proliferation-related proteins PCNA, Ki67, CyclinD1, CDK-2, and CDK-6
Ki-67↓,
cycD1/CCND1↓,
CDK2↑,
CDK6↓,
Bcl-2↓,
cl‑PARP↑, up-regulated the expression of cleaved PARP, Bax, Active Caspase3, DR4, and DR5
BAX↑,
Casp3↑,
DR4↑,
DR5↑,
Snail↓, down-regulated the expression of Snail, MMP-2, and MMP-9
MMP2↓,
MMP9↓,
TGF-β↑, up-regulation of TGF-β1
PKCδ↓, Inhibition of PKC signaling
β-catenin/ZEB1↓, decreases the expression level of β-catenin
SIRT1↓, down-regulates the expression of anti-apoptotic protein, SIRT1, HuR, and HO-1 protein
HO-1↓,
ROS↑, up-regulates ROS
CHOP↑, activating the CHOP signaling pathway to induce apoptosis
Cyt‑c↑, releases cytochrome c
MMP↓, decreases mitochondrial membrane potential and oxygen consumption,
OCR↓,
AMPK↑, activates AMPK, and downregulates HIF-1α expression
Hif1a↓,
NF-kB↓, inhibition of NF-κB pathway
E-cadherin↑, Upregulates E-cadherin, downregulates vimentin and then blocks EMT progression
Vim↓,
EMT↓,
LC3II↑, Up-regulation of LC3 – II expression and down-regulation of CIP2A
CIP2A↓,
GLUT1↓, regulation of glycolysis-related gene GLUT1 and downstream protein PDH expression
PDH↝,
MAD↓, Downregulation of MAD, LDH, GR, GST, and GSH-Px related protein expressio
LDH↓,
GSTs↑,
NOTCH↓, inhibited the expression of Akt and Notch protein
survivin↓, survivin and XIAP was also significantly down-regulated
XIAP↓,
ER Stress↑, through ER stress
ChemoSideEff↓, could improve cisplatin-induced hepatotoxicity in colorectal cancer cells
ChemoSen↑, Enhancing chemosensitivity
AntiCan↑, The anticancer potential of lycopene has been described by various in vitro cells, animal studies, and some clinical trials.
antiOx↓, anticancer potential of lycopene is mainly due to its powerful singlet-oxygen quencher characteristics, simulation of detoxifying/antioxidant enzymes production,
Apoptosis↓, initiation of apoptosis, inhibition of cell proliferation and cell cycle progression as well as modulations of gap junctional communication, the growth factors, and signal transduction pathways
TumCP↓,
TumCCA↑,
Risk↓, The link between increased lycopene consumption and reducedoccurrence of a variety of cancers has been documented by in vitro cells,animal studies, and some clinical studies.
ROS↓, The antioxidant action of lycopene toward ROS
SOD↑, Lycopene can simulate detoxifying/antioxidant enzyme productionsuch as superoxide dismutase (SOD), catalase (CAT), glutathione-S-transferase (GST), and glutathione reductase.
Catalase↑, . By stimulating ARE system, the lycopene can increase detoxifying/antioxidant enzymes production such as SOD, CAT, GST
GSTs↑,
ARE↑, The upregulating of the ARE system by lycopere has been studied in human BEAS-2B, HepG2, and MCF7
NRF2↑, figure 1
cycD1/CCND1↓, figure 2
cycE/CCNE↑,
CDK2↑,
p27↑,
BAX↑,
Bcl-2↓,
P53↑,
ChemoSen↑, Lycopene has also been declared to have a synergistic effect with drugs used in cancer treatment [16,17,27,32]. Lycopene may contribute to improved anticancer effects of enzalutamide
FAK↓, Quercetin can inhibit HGF-induced melanoma cell migration by inhibiting the activation of c-Met and its downstream Gabl, FAK and PAK [84]
TumCCA↑, stimulation of cell cycle arrest at the G1 stage
p‑pRB↓, mediated through regulation of p21 CDK inhibitor and suppression of pRb phosphorylation resulting in E2F1 sequestering.
CDK2↑, low dose of quercetin has brought minor DNA injury and Chk2 induction
CycB/CCNB1↓, quercetin has a role in the reduction of cyclin B1 and CDK1 levels,
CDK1↓,
EMT↓, quercetin suppresses epithelial to mesenchymal transition (EMT) and cell proliferation through modulation of Sonic Hedgehog signaling pathway
PI3K↓, quercetin on other pathways such as PI3K, MAPK and WNT pathways have also been validated in cervical cancer
MAPK↓,
Wnt↓,
ROS↑, colorectal cancer, quercetin has been shown to suppress carcinogenesis through various mechanisms including affecting cell proliferation, production of reactive oxygen species and expression of miR-21
miR-21↑,
Akt↓, Figure 1 anti-cancer mechanisms
NF-kB↓,
FasL↑,
Bak↑,
BAX↑,
Bcl-2↓,
Casp3↓,
Casp9↑,
P53↑,
p38↑,
MAPK↑,
Cyt‑c↑,
PARP↓,
CHOP↑,
ROS↓,
LDH↑,
GRP78/BiP↑,
ERK↑,
MDA↓,
SOD↑,
GSH↑,
NRF2↑,
VEGF↓,
PDGF↓,
EGF↓,
FGF↓,
TNF-α↓,
TGF-β↓,
VEGFR2↓,
EGFR↓,
FGFR1↓,
mTOR↓,
cMyc↓,
MMPs↓,
LC3B-II↑,
Beclin-1↑,
IL1β↓,
CRP↓,
IL10↓,
COX2↓,
IL6↓,
TLR4↓,
Shh↓,
HER2/EBBR2↓,
NOTCH↓,
DR5↑, quercetin has enhanced DR5 expression in prostate cancer cells
HSP70/HSPA5↓, Quercetin has also suppressed the upsurge of hsp70 expression in prostate cancer cells following heat treatment and enhanced the quantity of subG1 cells
CSCs↓, Quercetin could also suppress cancer stem cell attributes and metastatic aptitude of isolated prostate cancer cells through modulating JNK signaling pathway
angioG↓, Quercetin inhibits angiogenesis-mediated of human prostate cancer cells through negatively modulating angiogenic factors (TGF-β, VEGF, PDGF, EGF, bFGF, Ang-1, Ang-2, MMP-2, and MMP-9)
MMP2↓,
MMP9↓,
IGFBP3↑, Quercetin via increasing the level of IGFBP-3 could induce apoptosis in PC-3 cells
uPA↓, Quercetin through decreasing uPA and uPAR expression and suppressing cell survival protein and Ras/Raf signaling molecules could decrease prostate cancer progression
uPAR↓,
RAS↓,
Raf↓,
TSP-1↑, Quercetin through TSP-1 enhancement could effectively inhibit angiogenesis
*antiOx↑, esame oil has been shown to have antioxidant and health-promoting benefits due to its high concentration of tocopherol, phytosterol, lignan, and other components
*LDL↓, sesame oil can reduce levels of low-density lipoprotein (LDL) and decrease the risk of atherosclerosis and cardiovascular diseases.
*Aβ↓, Alzheimer’s disease is linked to the deposition of toxic cellular amyloid proteins, and the prolonged consumption of sesamol may efficiently hinder this buildup
*TNF-α↓, Figure 2
*SOD↑,
*SIRT1↑,
*Catalase↑,
*GSH↑,
*MDA↓,
*GSTs↑,
*IL4↑,
*GPx↑,
*COX2↓,
*PGE2↓,
*NO↓,
CDK2↑,
COX2↑,
MMP9↑,
ICAM-1↓,
*BDNF↑, sesame oil increased brain-derived neurotrophic factor (BDNF) and peroxisome proliferator-activated receptor gamma (PPAR-γ) levels.
*PPARγ↑,
*AChE↓, figure 2
*Inflam↓, potent antioxidant properties, which may contribute to its anti-inflammatory effects.
*HO-1↑, activation of HO-1, leading to the inhibition of the IKKα/NFκB pathway, recognized for its involvement in inflammatory processes
*NF-kB↓,
*ROS↓, sesamin was found to decrease oxidative stress markers, including malondialdehyde (MDA) and reactive oxygen species (ROS), and increase the activity of antioxidant enzymes, such as superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px).
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in-vitro, |
Pca, |
DU145 |
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in-vitro, |
Pca, |
PC3 |
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TumCG↓,
TumCP↓,
TumCCA↑, cell cycle arrest at the S- and G2/M-phase
H3↑,
H4↑,
HDAC↓, SFN acts as a histone deacetylase (HDAC) inhibitor.
CDK1↑, With 10 µM SFN, CDK1 and CDK2 increased in both cell lines,
CDK2↑,
p19↑,
*BioAv↑, A transient decrease in HDAC activity has also been observed in healthy humans 3 h after providing a daily 200 µM SFN dose, resulting in a plasma concentration of SFN metabolites of 0.1–0.2 µM
Showing Research Papers: 1 to 6 of 6
* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 6
Pathway results for Effect on Cancer / Diseased Cells:
Redox & Oxidative Stress ⓘ
antiOx↓, 1, ARE↑, 1, Catalase↑, 1, Ferroptosis↑, 1, GSH↑, 1, GSTs↑, 2, HO-1↓, 1, lipid-P↑, 1, MAD↓, 1, MDA↓, 1, NRF2↑, 2, ROS↓, 2, ROS↑, 3, SOD↑, 2,
Metal & Cofactor Biology ⓘ
Ferritin↓, 1, Tf↑, 1,
Mitochondria & Bioenergetics ⓘ
EGF↓, 1, FGFR1↓, 1, MMP↓, 1, OCR↓, 1, Raf↓, 1, XIAP↓, 1,
Core Metabolism/Glycolysis ⓘ
AMPK↑, 2, cMyc↓, 1, LDH↓, 1, LDH↑, 1, PDH↝, 1, SIRT1↓, 1, SIRT1↑, 1,
Cell Death ⓘ
Akt↓, 2, Apoptosis↓, 1, Apoptosis↑, 2, Bak↑, 1, BAX↑, 3, Bcl-2↓, 3, Casp3↓, 1, Casp3↑, 1, Casp9↑, 1, Cyt‑c↑, 2, DR4↑, 1, DR5↑, 2, FasL↑, 1, Ferroptosis↑, 1, MAPK↓, 2, MAPK↑, 1, p27↑, 1, p38↑, 1, survivin↓, 2,
Kinase & Signal Transduction ⓘ
HER2/EBBR2↓, 1,
Transcription & Epigenetics ⓘ
H3↑, 1, H4↑, 1, miR-21↑, 1, p‑pRB↓, 1,
Protein Folding & ER Stress ⓘ
CHOP↑, 2, ER Stress↑, 1, GRP78/BiP↑, 1, HSP70/HSPA5↓, 1,
Autophagy & Lysosomes ⓘ
Beclin-1↑, 1, LC3B-II↑, 1, LC3II↑, 1, TumAuto↑, 2,
DNA Damage & Repair ⓘ
DNAdam↑, 1, P53↑, 2, PARP↓, 1, cl‑PARP↑, 1, PCNA↓, 1,
Cell Cycle & Senescence ⓘ
CDK1↓, 1, CDK1↑, 2, CDK2↑, 6, CDK4↑, 1, CycB/CCNB1↓, 1, cycD1/CCND1↓, 2, cycE/CCNE↑, 1, p19↑, 1, TumCCA↑, 4,
Proliferation, Differentiation & Cell State ⓘ
CIP2A↓, 1, CSCs↓, 1, Diff↑, 1, EMT↓, 2, ERK↑, 1, FGF↓, 1, HDAC↓, 1, IGFBP3↑, 1, mTOR↓, 1, mTOR↑, 1, NOTCH↓, 3, PI3K↓, 2, RAS↓, 1, Shh↓, 1, TumCG↓, 1, Wnt↓, 1,
Migration ⓘ
E-cadherin↑, 1, FAK↓, 1, Ki-67↓, 1, MMP2↓, 2, MMP9↓, 2, MMP9↑, 1, MMPs↓, 1, PDGF↓, 1, PKCδ↓, 1, Snail↓, 1, TGF-β↓, 1, TGF-β↑, 1, TSP-1↑, 1, TumCI↓, 2, TumCMig↓, 1, TumCP↓, 4, TumMeta↓, 1, uPA↓, 1, uPAR↓, 1, Vim↓, 1, β-catenin/ZEB1↓, 1,
Angiogenesis & Vasculature ⓘ
angioG↓, 2, EGFR↓, 1, Hif1a↓, 1, VEGF↓, 1, VEGFR2↓, 2,
Barriers & Transport ⓘ
GLUT1↓, 1,
Immune & Inflammatory Signaling ⓘ
COX2↓, 2, COX2↑, 1, CRP↓, 1, ICAM-1↓, 1, IL10↓, 1, IL1β↓, 2, IL6↓, 1, NF-kB↓, 2, PD-1↓, 1, TLR4↓, 1, TNF-α↓, 1,
Hormonal & Nuclear Receptors ⓘ
CDK6↓, 1, CDK6↑, 1,
Drug Metabolism & Resistance ⓘ
ChemoSen↑, 3, RadioS↑, 1,
Clinical Biomarkers ⓘ
CRP↓, 1, EGFR↓, 1, Ferritin↓, 1, HER2/EBBR2↓, 1, IL6↓, 1, Ki-67↓, 1, LDH↓, 1, LDH↑, 1,
Functional Outcomes ⓘ
AntiCan↑, 2, ChemoSideEff↓, 1, Risk↓, 1,
Total Targets: 144
Pathway results for Effect on Normal Cells:
Redox & Oxidative Stress ⓘ
antiOx↑, 1, Catalase↑, 1, GPx↑, 1, GSH↑, 1, GSTs↑, 1, HO-1↑, 1, MDA↓, 1, ROS↓, 1, SOD↑, 1,
Core Metabolism/Glycolysis ⓘ
LDL↓, 1, PPARγ↑, 1, SIRT1↑, 1,
Angiogenesis & Vasculature ⓘ
NO↓, 1,
Immune & Inflammatory Signaling ⓘ
COX2↓, 1, IL4↑, 1, Inflam↓, 1, NF-kB↓, 1, PGE2↓, 1, TNF-α↓, 1,
Synaptic & Neurotransmission ⓘ
AChE↓, 1, BDNF↑, 1,
Protein Aggregation ⓘ
Aβ↓, 1,
Drug Metabolism & Resistance ⓘ
BioAv↑, 1,
Total Targets: 23
Scientific Paper Hit Count for: CDK2, Cyclin-dependent kinase 2
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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