CHK1 Cancer Research Results

CHK1, Checkpoint Kinase 1: Click to Expand ⟱
Source:
Type:
A protein that plays a crucial role in the DNA damage response pathway. It is involved in the repair of DNA damage and the maintenance of genome stability.
CHK1 acts as a tumor suppressor by preventing the accumulation of DNA damage and maintaining genome stability. Loss of CHK1 function can lead to increased genetic instability and a higher risk of cancer.
-CHK1 is often overexpressed in various types of cancer, including breast, colorectal, lung, and ovarian cancer. Overexpression of CHK1 can contribute to the development of resistance to chemotherapy and radiation therapy.
-CHK1 expression is often higher in tumor cells compared to normal cells. This tumor-specific expression makes CHK1 a potential target for cancer therapy.
Scientific Papers found: Click to Expand⟱
251- AL,    Inhibition of allicin in Eca109 and EC9706 cells via G2/M phase arrest and mitochondrial apoptosis pathway
- in-vitro, ESCC, Eca109 - in-vitro, ESCC, EC9706 - in-vivo, NA, NA
Apoptosis↑,
P53↑,
P21↑,
CHK1↑,
CycB/CCNB1↓,
BAX↑,
Casp3↑,
Casp9↑,
Cyt‑c↑, allicin treatment resulted in Cyt c release from the mitochondria to the cytosol.

310- Api,    Apigenin inhibits renal cell carcinoma cell proliferation
- vitro+vivo, RCC, ACHN - in-vitro, RCC, 786-O - in-vitro, RCC, Caki-1 - in-vitro, RCC, HK-2
TumCCA↑, G2/M cell cycle arrest.
p‑ATM↑, p-ATM
p‑CHK1↑, p-Chk2
p‑CDC25↑, p-Cdc25c
p‑cDC2↑, phosphorylated Cdc2 (p-Cdc2 on tyrosine15), also increased
P53↑, 10, 20, 40 uM
BAX↑,
Casp9↑,
Casp3↑,

556- ART/DHA,    Artemisinins as a novel anti-cancer therapy: Targeting a global cancer pandemic through drug repurposing
- Review, NA, NA
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↓,

5808- CPT,    Repair of Topoisomerase I-Mediated DNA Damage
- Review, Var, NA
TOP1↓, Top1 is the selective target of camptothecins, which are effective anticancer agents.
AntiCan↑,
Dose?, Two camptothecin derivatives are used in cancer therapy: hycamtin (Topotecan®) and CPT-11 (Irinotecan; Camptosar®) [31].
CHK1↑, Chk1 activation by camptothecin
Chk2↑, Chk2 activation by camptothecin

1655- FA,    Ferulic acid inhibiting colon cancer cells at different Duke’s stages
- in-vitro, Colon, SW480 - in-vitro, Colon, Caco-2 - in-vitro, Colon, HCT116
TumCP↓, ferulic acid significantly inhibits the proliferation and migration of these cells
TumCMig↓,
TumCCA↑, ferulic acid significantly inhibits the proliferation and migration of these cells
Apoptosis↑,
ATM↑, ferulic acid activates the ATM/Chk2 and ATR/Chk1 pathways
Chk2↑,
ATR↑,
CHK1↑,
CK2↓, down regulating their relative cell cycle regulatory proteins (CDK2 and Cyclin A2 complex, CDK4/6 and Cyclin D1/E1 complex)
cycA1/CCNA1↑, Cyclin A2 complex
CDK4↓,
CDK6↓,
cycD1/CCND1↓,
cycE/CCNE↓,
P53↑,
P21↑,

2827- FIS,    The Potential Role of Fisetin, a Flavonoid in Cancer Prevention and Treatment
- Review, Var, NA
*antiOx↑, effective antioxidant, anti-inflammatory
*Inflam↓,
neuroP↑, neuro-protective, anti-diabetic, hepato-protective and reno-protective potential.
hepatoP↑,
RenoP↑,
cycD1/CCND1↓, Figure 3
TumCCA↑,
MMPs↓,
VEGF↓,
MAPK↓,
NF-kB↓,
angioG↓,
Beclin-1↑,
LC3s↑,
ATG5↑,
Bcl-2↓,
BAX↑,
Casp↑,
TNF-α↓,
Half-Life↓, Fisetin was given at an effective dosage of 223 mg/kilogram intraperitoneally in mice. The plasma concentration declined biophysically, with a rapid half-life of 0.09 h and a terminal half-life of 3.1 h,
MMP↓, Fisetin powerfully improved apoptotic cells and caused the depolarization of the mitochondrial membrane.
mt-ROS↑, Fisetin played a role in the induction of apoptosis, independently of p53, and increased mitochondrial ROS generation.
cl‑PARP↑, fisetin-induced sub-G1 population as well as PARP cleavage.
CDK2↓, Moreover, the activities of cyclin-dependent kinases (CDK) 2 as well as CDK4 were decreased by fisetin and also inhibited CDK4 activity in a cell-free system, demonstrating that it might directly inhibit the activity of CDK4
CDK4↓,
Cyt‑c↑, Moreover, release of cytochrome c and Smac/Diablo was induced by fisetin
Diablo↑,
DR5↑, Fisetin caused an increase in the protein levels of cleaved caspase-8, DR5, Fas ligand, and TNF-related apoptosis-inducing ligand
Fas↑,
PCNA↓, Fisetin decreased proliferation-related proteins such as PCNA, Ki67 and phosphorylated histone H3 (p-H3) and decreased the expression of cell growth
Ki-67↓,
p‑H3↓,
chemoP↑, Paclitaxel treatment only showed more toxicity to normal cells than the combination of flavonoids with paclitaxel, suggesting that fisetin might bring some safety against paclitaxel-facilitated cytotoxicity.
Ca+2↑, Fisetin encouraged apoptotic cell death via increased ROS and Ca2+, while it increased caspase-8, -9 and -3 activities and reduced the mitochondrial membrane potential in HSC3 cells.
Dose↝, After fisetin treatment at 40 µM, invasion was reduced by 87.2% and 92.4%, whereas after fisetin treatment at 20 µM, invasion was decreased by 52.4% and 59.4% in SiHa and CaSki cells, respectively
CDC25↓, This study proposes that fisetin caused the arrest of the G2/M cell cycle via deactivating Cdc25c as well Cdc2 via the activation of Chk1, 2 and ATM
CDC2↓,
CHK1↑,
Chk2↑,
ATM↑,
PCK1↓, fisetin decreases the levels of SOS-1, pEGFR, GRB2, PKC, Ras, p-p-38, p-ERK1/2, p-JNK, VEGF, FAK, PI3K, RhoA, p-AKT, uPA, NF-ĸB, MMP-7,-9 and -13, whereas it increases GSK3β as well as E-cadherin in U-2 OS
RAS↓,
p‑p38↓,
Rho↓,
uPA↓,
MMP7↓,
MMP13↓,
GSK‐3β↑,
E-cadherin↑,
survivin↓, whereas those of survivin and BCL-2 were reduced in T98G cells
VEGFR2↓, Fisetin inhibited the VEGFR expression in Y79 cells as well as the angiogenesis of a tumor.
IAP2↓, The downregulation of cIAP-2 by fisetin
STAT3↓, fisetin induced apoptosis in TPC-1 cells via the initiation of oxidative damage and enhanced caspases expression by downregulating STAT3 and JAK 1 signaling
JAK1↓,
mTORC1↓, Fisetin acts as a dual inhibitor of mTORC1/2 signaling,
mTORC2↓,
NRF2↑, Moreover, In JC cells, the Nrf2 expression was gradually increased by fisetin from 8 h to 24 h

924- RES,    Resveratrol sequentially induces replication and oxidative stresses to drive p53-CXCR2 mediated cellular senescence in cancer cells
- in-vitro, OS, U2OS - in-vitro, Lung, A549
TumCCA↑, S-phase arrest, which is commonly observed in cells treated with RSV
ROS↑,
γH2AX↑, remarkable increase in the amount of γ-H2AX, a marker for DNA double-strand breaks
ATM↑, a master regulator of DNA damage response, was activated by RSV
p‑CHK1↑,
cellSen↑,
CXCR2↑, peaks at day 5 then drops


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 ⓘ

Ferroptosis↑, 1,   NRF2↑, 1,   ROS↑, 2,   mt-ROS↑, 1,  

Mitochondria & Bioenergetics ⓘ

CDC2↓, 1,   CDC25↓, 1,   p‑CDC25↑, 1,   MMP↓, 1,  

Core Metabolism/Glycolysis ⓘ

cMyc↓, 1,   PCK1↓, 1,  

Cell Death ⓘ

Akt↓, 1,   Apoptosis↑, 3,   BAX↑, 3,   Bcl-2↓, 1,   Casp↑, 1,   Casp3↑, 2,   Casp9↑, 2,   Chk2↑, 3,   p‑Chk2↑, 1,   CK2↓, 1,   Cyt‑c↑, 2,   Diablo↑, 1,   DR5↑, 1,   Fas↑, 1,   Ferroptosis↑, 1,   IAP2↓, 1,   MAPK↓, 1,   oncosis↑, 1,   p27↑, 1,   p‑p38↓, 1,   survivin↓, 2,  

Transcription & Epigenetics ⓘ

p‑H3↓, 1,  

Autophagy & Lysosomes ⓘ

ATG5↑, 1,   Beclin-1↑, 1,   LC3s↑, 1,   TumAuto↑, 1,  

DNA Damage & Repair ⓘ

ATM↑, 3,   p‑ATM↑, 2,   ATR↑, 1,   p‑ATR↑, 1,   CHK1↑, 4,   p‑CHK1↑, 3,   DNAdam↑, 1,   HR↓, 1,   p16↑, 1,   P53↑, 3,   cl‑PARP↑, 1,   PCNA↓, 1,   RAD51↓, 1,   γH2AX↑, 1,  

Cell Cycle & Senescence ⓘ

CDK2↓, 1,   CDK4↓, 2,   cycA1/CCNA1↑, 1,   CycB/CCNB1↓, 1,   cycD1/CCND1↓, 3,   cycE/CCNE↓, 1,   cycE1↓, 1,   P21↑, 2,   TumCCA↑, 5,  

Proliferation, Differentiation & Cell State ⓘ

p‑cDC2↑, 1,   cMET↓, 1,   ERK↓, 1,   GSK‐3β↑, 1,   mTOR↓, 1,   mTORC1↓, 1,   mTORC2↓, 1,   PI3K↓, 1,   RAS↓, 1,   STAT3↓, 1,   TOP1↓, 1,   Wnt/(β-catenin)↓, 1,  

Migration ⓘ

Ca+2↑, 1,   CDK4/6↓, 1,   E-cadherin↑, 1,   ITGB1↑, 1,   Ki-67↓, 1,   MMP13↓, 1,   MMP2↓, 1,   MMP7↓, 1,   MMPs↓, 1,   NCAM↑, 1,   Rho↓, 1,   TGF-β↓, 1,   TIMP2↑, 1,   TumCMig↓, 1,   TumCP↓, 1,   uPA↓, 1,  

Angiogenesis & Vasculature ⓘ

angioG↓, 1,   EGFR↓, 1,   Hif1a↓, 1,   KDR/FLK-1↓, 1,   NO↓, 1,   VEGF↓, 2,   VEGFR2↓, 1,  

Immune & Inflammatory Signaling ⓘ

cellSen↑, 1,   CXCR2↑, 1,   IL1↓, 1,   IL6↓, 1,   JAK1↓, 1,   MIP2↓, 1,   NF-kB↓, 2,   PGE2↓, 1,   TNF-α↓, 2,  

Hormonal & Nuclear Receptors ⓘ

CDK6↓, 1,  

Drug Metabolism & Resistance ⓘ

Dose?, 1,   Dose↝, 1,   Half-Life↓, 1,  

Clinical Biomarkers ⓘ

EGFR↓, 1,   IL6↓, 1,   Ki-67↓, 1,  

Functional Outcomes ⓘ

AntiCan↑, 1,   chemoP↑, 1,   hepatoP↑, 1,   neuroP↑, 1,   RenoP↑, 1,  
Total Targets: 115

Pathway results for Effect on Normal Cells:


Redox & Oxidative Stress ⓘ

antiOx↑, 1,  

Immune & Inflammatory Signaling ⓘ

Inflam↓, 1,  
Total Targets: 2

Scientific Paper Hit Count for: CHK1, Checkpoint Kinase 1
1 Allicin (mainly Garlic)
1 Apigenin (mainly Parsley)
1 Artemisinin
1 Camptothecin
1 Ferulic acid
1 Fisetin
1 Resveratrol
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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