ATR Cancer Research Results

ATR, Ataxia-Telangiectasia and Rad3-related: Click to Expand ⟱
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ATR (Ataxia-Telangiectasia and Rad3-related) is a serine/threonine kinase that plays a crucial role in maintaining genome stability and preventing cancer.

ATR is a protein kinase that is activated in response to DNA damage, particularly replication stress and single-strand breaks. When DNA damage occurs, ATR is activated and phosphorylates a variety of downstream targets, including Chk1, p53, and BRCA1. This activation of ATR triggers a signaling cascade that leads to cell cycle arrest, DNA repair, and apoptosis (programmed cell death) if the damage is too severe to be repaired.
ATR is frequently overexpressed in cancers, and its expression is associated with a more aggressive disease and poorer outcomes.
Scientific Papers found: Click to Expand⟱
7462- ,    Neuroprotective effects of honokiol: from chemistry to medicine
- Study, AD, NA
*ATR↑, Honokiol can permeate the blood brain barrier and the blood-cerebrospinal fluid to increase its bioavailability in neurological tissues.
*neuroP↑, Diverse studies have provided evidence on the neuroprotective effect of honokiol in the central nervous system, due to its potent antioxidant activity
*antiOx↑,
*Inflam↓, reduction in neuroinflammation
*Half-Life↝, rodent model [19]. The injection of 5–10 mg kg21 of honokiol has a plasma t1/2 value of 40–60 min, while the intraperitoneal injection in mice of 250 mg kg21 resulted in t1/2 value of 4–6 h, with a tmax of about 20–30 min
*ROS↓, fig 3
*Ca+2↓, demonstrated that honokiol counteracted Ab1–40 -induced elevation of Ca21, which is in strong agreement tothe antioxidative properties of honokiol
*GABA↓,
*COX2/PTGS2↓,
*memory↑, administration of ethanol extract of Magnolia officinalis (5 and 10 mg kg21 ) for 7 days improves the spatial long-term memory in scopolamine-induced mouse model of amnesia

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↓,
VEGFR2/KDR/Flk1↓,
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/CDKN1B↑,
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↓,

5651- BNL,  Cisplatin,    Natural borneol sensitizes human glioma cells to cisplatin-induced apoptosis by triggering ROS-mediated oxidative damage and regulation of MAPKs and PI3K/AKT pathway
- in-vitro, GBM, U251 - in-vitro, GBM, U87MG
ChemoSen↑, NB synergistically enhanced the anticancer efficacy of cisplatin in human glioma cells.
tumCV↓, Co-treatment of 40 μg/mL NB and 40 μg/mL cisplatin significantly inhibited U251 cell viability from 100% to 28.2% and increased the sub-G1 population from 1.4% to 59.3%.
TumCCA↑,
Apoptosis↑, NB enhanced cisplatin-induced apoptosis by activating caspases and triggering reactive oxygen species (ROS) overproduction
ROS↑,
DNAdam↑, ROS-mediated DNA damage was observed as reflected by the activation of ATM/ATR, p53 and histone.
ATR↑,
ATM↑,
P53↑,
Histones↑,
eff↓, ROS inhibition by antioxidants effectively improved MAPKs and PI3K/AKT functions and cell viability, indicating that NB enhanced cisplatin-induced cell growth in a ROS-dependent manner.
Casp3↑, the activation of caspase −3, −7, and −9 was further enhanced after the combination of 40 µg/mL of NB
Casp7↑,
Casp9↑,

454- CUR,    Curcumin-Induced DNA Demethylation in Human Gastric Cancer Cells Is Mediated by the DNA-Damage Response Pathway
- in-vitro, GC, MGC803
TumCMig↓,
TumCP↓,
ROS↑,
mtDam↑,
DNAdam↑,
Apoptosis↑,
ATR↑,
P21↑,
p‑P53↑,
GADD45A↑,
p‑γH2AX↑,

7507- FA,    Assessment of the anticancer mechanism of ferulic acid via cell cycle and apoptotic pathways in human prostate cancer cell lines
- in-vitro, Pca, LNCaP - in-vitro, Pca, PC3
Dose↝, The half maximal inhibitory concentration (IC50) dose of FA was found to be 300 μM in PC-3 cells and 500 μM in LNCaP cells.
ATR↑, FA inhibited cell proliferation by increasing the gene expressions of ATR, ATM, CDKN1A, CDKN1B, E2F4, RB1, and TP53
ATM↑,
P21↑,
p27/CDKN1B↑,
E2F4↑,
RB1↑,
TP53↑,
cycD1/CCND1↓, and decreasing the gene expressions of CCND1, CCND2, CCND3, CDK2, CDK4, and CDK6 in PC-3 cells.
CDK2↓,
CDK4↓,
CDK6↓,
TumCP↓, suppressed cell proliferation by increasing in the gene expressions of CASP1, CASP2, CASP8, CYCS, FAS, FASLG, and TRADD
Casp1↑,
Casp2↑,
Casp8↑,
Fas↑,
TRADD↑,
Bcl-2↓, and decreasing in the gene expressions of BCL2 and XIAP in LNCaP cells
XIAP↓,
TumCCA↑, FA may lead to cell cycle arrest in PC-3 cells while it may cause apoptosis in LNCaP cells.

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↑,


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:


NA, unassigned(tgid=0) ⓘ

E2F4↑, 1,   TRADD↑, 1,  

Redox & Oxidative Stress(tgid=1) ⓘ

Ferroptosis↑, 1,   ROS↑, 3,  

Mitochondria & Bioenergetics(tgid=3) ⓘ

mtDam↑, 1,   XIAP↓, 1,  

Core Metabolism/Glycolysis(tgid=4) ⓘ

cMyc↓, 1,   Histones↑, 1,  

Cell Death(tgid=5) ⓘ

Akt↓, 1,   Apoptosis↑, 4,   Bcl-2↓, 1,   Casp1↑, 1,   Casp2↑, 1,   Casp3↑, 1,   Casp7↑, 1,   Casp8↑, 1,   Casp9↑, 1,   Chk2↑, 1,   p‑Chk2↑, 1,   CK2↓, 1,   Fas↑, 1,   Ferroptosis↑, 1,   oncosis↑, 1,   p27/CDKN1B↑, 2,   survivin↓, 1,  

Transcription & Epigenetics(tgid=7) ⓘ

tumCV↓, 1,  

Autophagy & Lysosomes(tgid=9) ⓘ

TumAuto↑, 1,  

DNA Damage & Repair(tgid=10) ⓘ

ATM↑, 3,   p‑ATM↑, 1,   ATR↑, 4,   p‑ATR↑, 1,   CHK1↑, 1,   p‑CHK1↑, 1,   DNAdam↑, 3,   GADD45A↑, 1,   HR↓, 1,   p16↑, 1,   P53↑, 2,   p‑P53↑, 1,   RAD51↓, 1,   TP53↑, 1,   p‑γH2AX↑, 1,  

Cell Cycle & Senescence(tgid=11) ⓘ

CDK2↓, 1,   CDK4↓, 2,   cycA1/CCNA1↑, 1,   cycD1/CCND1↓, 3,   cycE/CCNE↓, 1,   cycE1↓, 1,   P21↑, 3,   RB1↑, 1,   TumCCA↑, 4,  

Proliferation, Differentiation & Cell State(tgid=12) ⓘ

cMET↓, 1,   ERK↓, 1,   mTOR↓, 1,   PI3K↓, 1,   Wnt/(β-catenin)↓, 1,  

Migration(tgid=13) ⓘ

CDK4/6↓, 1,   ITGB1↑, 1,   MMP2↓, 1,   NCAM↑, 1,   TGF-β↓, 1,   TIMP2↑, 1,   TumCMig↓, 2,   TumCP↓, 3,  

Angiogenesis & Vasculature(tgid=14) ⓘ

EGFR↓, 1,   Hif1a↓, 1,   NO↓, 1,   VEGF↓, 1,   VEGFR2/KDR/Flk1↓, 1,  

Immune & Inflammatory Signaling(tgid=16) ⓘ

IL1↓, 1,   IL6↓, 1,   MIP2↓, 1,   NF-kB↓, 1,   PGE2↓, 1,   TNF-α↓, 1,  

Hormonal & Nuclear Receptors(tgid=20) ⓘ

CDK6↓, 2,  

Drug Metabolism & Resistance(tgid=21) ⓘ

ChemoSen↑, 1,   Dose↝, 1,   eff↓, 1,  

Clinical Biomarkers(tgid=22) ⓘ

EGFR↓, 1,   IL6↓, 1,   TP53↑, 1,  
Total Targets: 82

Pathway results for Effect on Normal Cells:


Redox & Oxidative Stress(tgid=1) ⓘ

antiOx↑, 1,   ROS↓, 1,  

DNA Damage & Repair(tgid=10) ⓘ

ATR↑, 1,  

Migration(tgid=13) ⓘ

Ca+2↓, 1,  

Immune & Inflammatory Signaling(tgid=16) ⓘ

COX2/PTGS2↓, 1,   Inflam↓, 1,  

Synaptic & Neurotransmission(tgid=18) ⓘ

GABA↓, 1,  

Drug Metabolism & Resistance(tgid=21) ⓘ

Half-Life↝, 1,  

Functional Outcomes(tgid=23) ⓘ

memory↑, 1,   neuroP↑, 1,  
Total Targets: 10

Scientific Paper Hit Count for: ATR, Ataxia-Telangiectasia and Rad3-related
2 Ferulic acid
1 Artemisinin
1 borneol
1 Cisplatin
1 Curcumin
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#:717  State#:%  Dir#:2
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