CDK1 Cancer Research Results

CDK1, Cyclin-dependent kinase 1: Click to Expand ⟱
Source:
Type:
CDK1, (Cyclin-dependent kinase 1) same as p34 (cdc2) kinase activity
Mitotic Gatekeeper, Essential Cell-Cycle Engine, and Therapeutic Vulnerability
Cell cycle control to gene expression regulation and apoptosis, CDK1 is intimately involved in many cellular events that are vital for cell survival.
CDK1 is a significant biomarker in various cancers, with its overexpression often correlating with aggressive tumor characteristics and poor prognosis. Targeting CDK1 may offer therapeutic potential, especially in cancers where its expression is linked to unfavorable outcomes.
Scientific Papers found: Click to Expand⟱
3396- ART/DHA,    Progress on the study of the anticancer effects of artesunate
- Review, Var, NA
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↑,

4817- ASTX,    Low Dose Astaxanthin Treatments Trigger the Hormesis of Human Astroglioma Cells by Up-Regulating the Cyclin-Dependent Kinase and Down-Regulated the Tumor Suppressor Protein P53
- in-vitro, GBM, U251
Dose⇅, At high concentrations (20–40 μM), AXT triggered apoptosis in U251-MG cells, as it has been previously shown in other cancer cell lines. However, low concentrations (4–8 μM) of AXT were found to upregulate the proliferative cell cycle.
ROS∅, low concentrations, AXT did not affect the intracellular ROS levels, while the superoxide dismutase activity increased moderately.
SOD↑,
CDK1↑, Low Dose Astaxanthin Treatments Trigger the Hormesis of Human Astroglioma Cells by Up-Regulating the Cyclin-Dependent Kinase and Down-Regulated the Tumor Suppressor Protein P53
P53↓,
TumCP⇅, we found that U251-MG cells show a biphasic response to AXT, that is low doses of AXT have a proliferative effect, with a maximum survival increase of 130.4 ± 2.4% after treatment with 5 µM of AXT, while AXT concentrations over 20 µM have an apoptoti
ROS↑, Treatment with High AXT Concentrations Increased Intracellular ROS Levels while Low AXT Concentrations did not Affect ROS Levels

6007- CGA,    A Comprehensive View on the Impact of Chlorogenic Acids on Colorectal Cancer
- Review, CRC, NA
antiOx↑, They are best known for their high concentration in coffee and other dietary sources and the antioxidant properties that they exhibit.
TumCCA↑, this review aims to enable a better understanding of the modes of action of chlorogenic acids in combating carcinogenesis, with a focus on cell cycle arrest, the induction of apoptosis, and the modulation of Wnt, Pi3K/Akt, and MAPK
Apoptosis↑,
Wnt↝,
PI3K↝,
MAPK↝,
ROS↓, CGAs have demonstrated significant reactive oxygen species (ROS) scavenging potential through two direct mechanisms: hydrogen atom transfer (HAT) and radical adduct formation (RAF)
BioAv↝, bioavailability of CGAs in humans involves a complex process of digestion, absorption, and metabolism (Figure 7), primarily occurring within the stomach, small and large intestines, governed by the interplay between host enzymes and gut microbiota
P53↑, ↑ p53, ↑ p21, ↑ p18, ↑ CDKI, ↓ cyclin-D1, ↑ G1 cell population
P21↑,
CDK1↑,
Ki-67↓, ↓ Ki-67
Ca+2↑, ↑ Ca2+ levels Caco-2—cell culture
p‑Akt↓, ↓ p-AKT, ↓ mTOR
mTOR↓,
GSH↑, ↑ GSH, ↑ Nrf-2, ↑ HO-1 Caco-2—cell culture
NRF2↑,
HO-1↑,
COX2↓, ↓ COX-2, ↓ TNF-α, ↓ IL-1β, ↓ IL-6 LPS-induced SW480—cell culture
TNF-α↓,
IL1β↓,
IL6↓,

1638- HCAs,    Anticancer potential of hydroxycinnamic acids: mechanisms, bioavailability, and therapeutic applications
- Review, Nor, NA
*BioAv↓, Hydroxycinnamic acids are sensitive compounds to the environment in the gastrointestinal track. They may interact with the components in the digestion system or can be affected by pH differences
Inflam↓, Hydroxycinnamic acids (p-coumaric, CAPE, chlorogenic, caffeic, and ferulic acids) exhibit anti-inflammatory activity both in vitro and in vivo
COX2↓, caffeic acid targets COX-2 and its product prostaglan-din E2
TumCCA↑, These phenolics can cause cell cycle arrest at various phases, including G1, S, S-G2, and G2.
ChemoSen↑, sensitize cancer cells to chemotherapy and radiation therapy.
RadioS↑,
selectivity↑, HCAs exhibit selective toxicity, with a higher propensity to induce cell death in cancerous cells compared to normal cells.
ROS↑, 100uM(CA) and 10mM(metforin) cervical Cancer, also 100uM@24hr in A549cells
DNAdam↑,
antiOx↑, Hydroxy-cinnamic acids have an antioxidant effect by suppressing reactive oxygen/nitrogen species (ROS/RNS) and superoxide dismutases (SODs) production
SOD↑,
Catalase↑,
GPx↑,
GSH↑,
NRF2↑,
NF-kB↓, In the promotion stage, these compounds possess anti-inflammatory effects, particularly by inhibit-ing nuclear factor kappa B (NF-kB)
Cyc↓,
CDK1↑, CDKs
P21↑,
p27↑,
P53↑,
VEGF↓,
MAPK↓,

1730- SFN,    Sulforaphane: An emergent anti-cancer stem cell agent
- Review, Var, NA
BioAv↓, When exposed to high temperatures during meal preparation, myrosinase can be degraded, lose its function, and subsequently compromise the synthesis of SFN.
BioAv↑, eating raw cruciferous vegetables, instead of heating them can significantly improve the biodisponibility of SFN and its subsequent beneficial effects.
GSTA1↑, induction of Phase II enzymes [glutathione S-transferase (GST)
P450↓, (cytochrome P450, CYP) inhibition
TumCCA↑, herb-derived agent can also promote cell cycle arrest and apoptosis by regulating different signaling pathways including Nuclear Factor erythroid Related Factor 2 (Nrf2)-Keap1 and NF-κB.
HDAC↓, modulate the activity of some epigenetic factors, such as histone deacetylases (HDAC),
P21↑, upregulation of p21 and p27,
p27↑,
DNMT1↓, SFN was able to decrease the expression of DNMT1 and DNMT3 in LnCap prostate cancer cells
DNMT3A↓,
cycD1/CCND1↑, reduce methylation in Cyclin D2 promoter, thus inducing Cyclin D2 gene expression in those cells
DNAdam↑, SFN induced DNA damage, enhanced Bax expression and the release of cytochrome C followed by apoptosis
BAX↑,
Cyt‑c↑,
Apoptosis↑,
ROS↑, SFN increased reactive oxygen species (ROS), apoptosis-inducing factor (AIF)
AIF↑,
CDK1↑,
Casp3↑, activation of caspase-3, -8, and -9
Casp8↑,
Casp9↑,
NRF2↑, SFN significantly activated the major antioxidant marker Nrf2 and decreased NFκB, TNF-α, IL-1β
NF-kB↓,
TNF-α↓,
IL1β↓,
CSCs↓, SFN, have attracted attention due to their anti-CSC effect
CD133↓,
CD44↓,
ALDH↓,
Nanog↓,
OCT4↓,
hTERT/TERT↓,
MMP2↓,
EMT↓, SFN was reported to inhibit EMT and metastasis in the NSCLC, the cell lines H1299
ALDH1A1↓, ALDH1A1), Wnt3, and Notch4, other CSC-related genes inhibited by SFN treatment
Wnt↓,
NOTCH↓, SFN can inhibit aberrantly activated embryonic pathways in CSCs, including Sonic Hedgehog (SHH), Wnt/β-catenin, Cripto-1 (CR-1), and Notch.
ChemoSen↑, These results suggest that the antioxidant properties of SFN do not impact the cytotoxicity of antineoplastic drugs, but on the contrary, seems to improve it.
*Ki-67↓, Ki-67 and HDAC3 levels significantly decreased in benign breast tissues, and there was also a reduction in HDAC activity in blood cells
*HDAC3↓,
*HDAC↓,

1463- SFN,    Sulforaphane induces reactive oxygen species-mediated mitotic arrest and subsequent apoptosis in human bladder cancer 5637 cells
- in-vitro, Bladder, 5637
tumCV↓,
CycB/CCNB1↑, concomitant increased complex between cyclin B1 and Cdk1
p‑CDK1↑, of cyclin B1 and phosphorylation of Cdk1
Apoptosis↑,
Casp8↑,
Casp9↑,
Casp3↑,
cl‑PARP↑,
ROS↑, maximum level of ROS accumulation was observed 3h after sulforaphane treatment.
eff↓, ROS scavenger, N-acetyl-L-cysteine, notably attenuated sulforaphane-mediated apoptosis as well as mitotic arrest

1453- SFN,    Sulforaphane Reduces Prostate Cancer Cell Growth and Proliferation In Vitro by Modulating the Cdk-Cyclin Axis and Expression of the CD44 Variants 4, 5, and 7
- in-vitro, Pca, DU145 - in-vitro, Pca, PC3
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 7 of 7

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 7

Pathway results for Effect on Cancer / Diseased Cells:


Redox & Oxidative Stress ⓘ

antiOx↑, 2,   Catalase↑, 1,   Ferroptosis↑, 1,   GPx↑, 1,   GSH↑, 2,   GSTA1↑, 1,   HO-1↑, 1,   lipid-P↑, 1,   NRF2↑, 3,   ROS↓, 1,   ROS↑, 5,   ROS∅, 1,   SOD↑, 2,  

Metal & Cofactor Biology ⓘ

Ferritin↓, 1,   Tf↑, 1,  

Mitochondria & Bioenergetics ⓘ

AIF↑, 1,  

Core Metabolism/Glycolysis ⓘ

AMPK↑, 1,   SIRT1↑, 1,  

Cell Death ⓘ

p‑Akt↓, 1,   Apoptosis↑, 4,   BAX↑, 1,   Casp3↑, 2,   Casp8↑, 2,   Casp9↑, 2,   Cyt‑c↑, 1,   Ferroptosis↑, 1,   hTERT/TERT↓, 1,   MAPK↓, 1,   MAPK↝, 1,   p27↑, 2,   survivin↓, 1,  

Transcription & Epigenetics ⓘ

H3↑, 1,   H4↑, 1,   tumCV↓, 1,  

Autophagy & Lysosomes ⓘ

TumAuto↑, 1,  

DNA Damage & Repair ⓘ

DNAdam↑, 3,   DNMT1↓, 1,   DNMT3A↓, 1,   P53↓, 1,   P53↑, 2,   cl‑PARP↑, 1,  

Cell Cycle & Senescence ⓘ

CDK1↑, 6,   p‑CDK1↑, 1,   CDK2↑, 2,   CDK4↑, 1,   Cyc↓, 1,   CycB/CCNB1↑, 1,   cycD1/CCND1↑, 1,   p19↑, 1,   P21↑, 3,   TumCCA↑, 5,  

Proliferation, Differentiation & Cell State ⓘ

ALDH↓, 1,   ALDH1A1↓, 1,   CD133↓, 1,   CD44↓, 1,   CSCs↓, 1,   Diff↑, 1,   EMT↓, 1,   HDAC↓, 2,   mTOR↓, 1,   mTOR↑, 1,   Nanog↓, 1,   NOTCH↓, 1,   OCT4↓, 1,   PI3K↝, 1,   TumCG↓, 1,   Wnt↓, 1,   Wnt↝, 1,  

Migration ⓘ

Ca+2↑, 1,   Ki-67↓, 1,   MMP2↓, 1,   TumCI↓, 1,   TumCMig↓, 1,   TumCP↓, 2,   TumCP⇅, 1,  

Angiogenesis & Vasculature ⓘ

angioG↓, 1,   VEGF↓, 1,  

Immune & Inflammatory Signaling ⓘ

COX2↓, 3,   IL1β↓, 3,   IL6↓, 1,   Inflam↓, 1,   NF-kB↓, 2,   TNF-α↓, 2,  

Hormonal & Nuclear Receptors ⓘ

CDK6↑, 1,  

Drug Metabolism & Resistance ⓘ

BioAv↓, 1,   BioAv↑, 1,   BioAv↝, 1,   ChemoSen↑, 3,   Dose⇅, 1,   eff↓, 1,   P450↓, 1,   RadioS↑, 2,   selectivity↑, 1,  

Clinical Biomarkers ⓘ

Ferritin↓, 1,   hTERT/TERT↓, 1,   IL6↓, 1,   Ki-67↓, 1,  
Total Targets: 97

Pathway results for Effect on Normal Cells:


Proliferation, Differentiation & Cell State ⓘ

HDAC↓, 1,   HDAC3↓, 1,  

Migration ⓘ

Ki-67↓, 1,  

Drug Metabolism & Resistance ⓘ

BioAv↓, 1,   BioAv↑, 1,  

Clinical Biomarkers ⓘ

Ki-67↓, 1,  
Total Targets: 6

Scientific Paper Hit Count for: CDK1, Cyclin-dependent kinase 1
3 Sulforaphane (mainly Broccoli)
1 Artemisinin
1 Astaxanthin
1 Chlorogenic acid
1 Hydroxycinnamic-acid
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#:382  State#:%  Dir#:2
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