Chk2 Cancer Research Results

Chk2, Checkpoint Kinase 2: Click to Expand ⟱

Source:

Type: protein

Chk2: a protein that plays a crucial role in the regulation of the cell cycle and the response to DNA damage. It is a tumor suppressor gene that helps to prevent cancer by ensuring that cells with damaged DNA do not divide and proliferate.
Chk2 is activated in response to DNA damage, such as that caused by ionizing radiation or certain chemicals. Once activated, Chk2 phosphorylates and activates other proteins that help to repair DNA damage or induce cell death (apoptosis) if the damage is too severe.
Decreased expression or loss of function of CHK2 is often associated with more aggressive tumor behavior, increased invasiveness, and poorer prognosis across various cancer types. CHK2 plays a crucial role in maintaining genomic stability, and its dysfunction can lead to increased susceptibility to DNA damage and tumorigenesis.

Scientific Papers found: Click to Expand⟱

556-

ART/DHA,

Artemisinins as a novel anti-cancer therapy: Targeting a global cancer pandemic through drug repurposing

Review,

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↓,

1520-

Ba,

Baicalein Induces G2/M Cell Cycle Arrest Associated with ROS Generation and CHK2 Activation in Highly Invasive Human Ovarian Cancer Cells

in-vitro,

Ovarian,

SKOV3

50–200 µM baicalein for 48 and 72 h

54uM

in-vitro,

Ovarian,

TOV-21G

91uM

TumCG↓,
TumCCA↑, G2/M phase
ROS↑, Baicalein-induced G2/M phase arrest is associated with an increased reactive oxygen species (ROS) production, DNA damage, and CHK2 upregulation and activation
DNAdam↑,
Chk2↑,
Dose∅, produced significant ROS in a dose- and time-dependent manner in SKOV-3 cells
p‑γH2AX↑, baicalein treatment increased the phosphorylation of H2AX (γH2AX)
CDC25↓,
CHK1↓,
cycD1/CCND1↓,
eff↓, CHK2 inhibitor indeed reduced the extent of CHK2 phosphorylation (Figure 4A) and protected SKOV-3 cells from baicalein-mediated G2/M arrest (Fig
12LOX↓, the pro-oxidative effect of baicalein, a specific inhibitor of 12-LOX, on ovarian cancer cells may occur through inhibiting the activity of 12-LOX, thereby inducing the accumulation of hydroxyl radicals.

5808-

CPT,

Repair of Topoisomerase I-Mediated DNA Damage

Review,

Var,

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

1328-

EMD,

Emodin induces apoptosis of human tongue squamous cancer SCC-4 cells through reactive oxygen species and mitochondria-dependent pathways

in-vitro,

Tong,

SCC4

TumCCA↑, G2/M arrest
P21↑,
Chk2↑,
CycB/CCNB1↓,
cDC2↓,
Apoptosis↑,
Cyt‑c↑, release of cytochrome c from mitochondria
Casp9↑,
Casp3↑,
ROS↑,
MMP↓,
Bax:Bcl2↑,
ER Stress↑,

1655-

FA,

Ferulic acid inhibiting colon cancer cells at different Duke’s stages

in-vitro,

Colon,

SW480

 0−400 μg/mL up to 72 h

176.41 ± 16.77ug/mL

in-vitro,

Colon,

Caco-2

179.19 ± 25.71ug/mL

in-vitro,

Colon,

HCT116

165.46 ± 5.87ug/mL

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,

*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

488-

MF,

Repetitive exposure to a 60-Hz time-varying magnetic field induces DNA double-strand breaks and apoptosis in human cells

in-vitro,

NA,

HeLa

60 Hz, 6 mT for 30 min every 24 h for 3 days

in-vitro,

NA,

IMR90

DNAdam↑,
p‑γH2AX↑,
Chk2↑,
p38↑,
Apoptosis↑, cancer and normal cell

487-

MF,

Extremely Low-Frequency Electromagnetic Fields Cause G1 Phase Arrest through the Activation of the ATM-Chk2-p21 Pathway

in-vitro,

NMSC,

HaCaT

60 Hz, 1.5 mT for 144 h

ATM↑,
Chk2↑,
P21↑,
TumCCA↑, cause G1 arrest and decrease colony formation

4944-

PEITC,

Phenethyl isothiocyanate induces DNA damage-associated G2/M arrest and subsequent apoptosis in oral cancer cells with varying p53 mutations

in-vitro,

Oral,

TumCG↓, PEITC was able to inhibit cell growth, arrest G2/M phase, and induce apoptosis of OSCC cells.
TumCCA↑, PEITC-induced G2/M phase arrest and apoptosis depend on the GSH redox stress- and p53-related pathway
Apoptosis↑,
ROS↑, PEITC induced reactive oxygen species and NO production, GSH depletion, and ΔΨm reduction in OSCC cells.
NO↑,
GSH↓,
MMP↓,
DNAdam↑, PEITC-induced oxidative DNA damage was associated with the activation of the ATM–Chk2–p53 pathway.
ATM↑,
Chk2↑,
P53↑,
eff↓, Pifithrin-α, NAC, or GSH, but not free radical scavengers, can reverse anticancer effects of PEITC.

913-

QC,

Effects of low dose quercetin: Cancer cell-specific inhibition of cell cycle progression

in-vitro,

BC,

SkBr3

in-vitro,

BC,

MDA-MB-435

TumCP↓,
TumCCA↑, arrest at the G1 phase
DNAdam↑, mild DNA damage
Chk2↑,
CycB/CCNB1↓, cyclin B1
CDK1↓,
tumCV↓, 94% viability with 10uM
p‑RB1↓, Rb
P21↑,

1434-

SFN,

GEM,

Sulforaphane Potentiates Gemcitabine-Mediated Anti-Cancer Effects against Intrahepatic Cholangiocarcinoma by Inhibiting HDAC Activity

in-vitro,

CCA,

HuCCT1

 SFN (0–80 μM) or GEM (0–10 μM) for 24 h

27.4uM(SFN),0.57 μM(GEM)

in-vitro,

CCA,

HuH28

34.2 μM(SFN), 0.71um(GEM)

in-vivo,

NA,

50 mg/kg/day

tumors of SFN- and GEM-treated mice

HDAC↓,
ac‑H3↑,
ChemoSen↑, SFN synergistically augmented the GEM-mediated attenuation of cell viability and proliferation
tumCV↓,
TumCP↓,
TumCCA↑, G2/M cell cycle arrest
Apoptosis↑,
cl‑Casp3↑,
TumCI↓,
VEGF↓, VEGFA
VEGFR2↓,
Hif1a↓,
eNOS↓,
EMT?, SFN effectively inhibited the GEM-mediated induction of epithelial–mesenchymal transition (EMT)
TumCG↓,
Ki-67↓,
TUNEL↑, increased TUNEL+ apoptotic cells
P21↑,
p‑Chk2↑,
CDC25↓, decreased p-Cdc25C
BAX↑,
*ROS↓, SFN is also known to exert anti-oxidative effects via Nrf2 activation. in vivo study, optimization is performed by evaluating the anti-oxidative property of SFN in the liver.
NQO1?, identified 50 mg/kg/day as the minimal dose that significantly induced these anti-oxidative genes

Showing Research Papers: 1 to 11 of 11

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 11

Pathway results for Effect on Cancer / Diseased Cells:

Pathway results for Effect on Normal Cells:

Redox & Oxidative Stress ⓘ

antiOx↑, 1, ROS↓, 1,

Immune & Inflammatory Signaling ⓘ

Inflam↓, 1,
Total Targets: 3

Scientific Paper Hit Count for: Chk2, Checkpoint Kinase 2

2 Magnetic Fields
1 Artemisinin
1 Baicalein
1 Camptothecin
1 Emodin
1 Ferulic acid
1 Fisetin
1 Phenethyl isothiocyanate
1 Quercetin
1 Sulforaphane (mainly Broccoli)
1 Gemcitabine (Gemzar)

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#:754  State#:%  Dir#:2
  wNotes=on  sortOrder:rid,rpid

Chk2 Cancer Research Results

Pathway results for Effect on Cancer / Diseased Cells:

Redox & Oxidative Stress ⓘ

Mitochondria & Bioenergetics ⓘ

Core Metabolism/Glycolysis ⓘ

Cell Death ⓘ

Transcription & Epigenetics ⓘ

Protein Folding & ER Stress ⓘ

Autophagy & Lysosomes ⓘ

DNA Damage & Repair ⓘ

Cell Cycle & Senescence ⓘ

Proliferation, Differentiation & Cell State ⓘ

Migration ⓘ

Angiogenesis & Vasculature ⓘ

Immune & Inflammatory Signaling ⓘ

Hormonal & Nuclear Receptors ⓘ

Drug Metabolism & Resistance ⓘ

Clinical Biomarkers ⓘ

Functional Outcomes ⓘ

Pathway results for Effect on Normal Cells:

Redox & Oxidative Stress ⓘ

Immune & Inflammatory Signaling ⓘ

Home Page