ATM Cancer Research Results

ATM, similar to Serine-protein kinase ATM (Ataxia telangiectasia mutated) (A-T, mutated); ataxia telangiectasia mutated: Click to Expand ⟱
Source: CGL-Driver Genes
Type: TSG
ATM is considered a moderate cancer risk gene. A mutation in a moderate risk gene is just one risk factor that can contribute to cancer development. ATM has traditionally been assigned the role of a tumor suppressor. However, in both humans and mice, lymphoma and leukemia are the only clear-cut examples of cancer development caused by ATM deficiency(13). Its roles in other types of cancer, especially solid tumors, are much less clear.
ATM, a master regulator of DNA damage response.
Scientific Papers found: Click to Expand⟱
3433- ALA,    Alpha lipoic acid promotes development of hematopoietic progenitors derived from human embryonic stem cells by antagonizing ROS signals
*ROS↓, However, in more mature hPSC‐derived hematopoietic stem/progenitor cells, ALA reduced ROS levels and inhibited apoptosis.
*Apoptosis↓,
*Hif1a↑, up‐regulating HIF1A in response to a hypoxic environment.
*FOXO1↑, ALA also up‐regulated sensor genes of ROS signals, including HIF1A, FOXO1, FOXO3, ATM, PETEN, SIRT1, and SIRT3, during the process of hPSCs derived hemogenic endothelial cells generation
*FOXO3↑,
*ATM↑,
*SIRT1↑,
*SIRT3↑,
*CD34↑, Flow cytometry analysis indicated that ALA improved the production of CD34+ CD43+ CD45+ hematopoietic stem/progenitor cells significantly

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↓,
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↓,

2674- BBR,    Berberine: A novel therapeutic strategy for cancer
- Review, Var, NA - Review, IBD, NA
Inflam↓, anti-inflammatory, antidiabetic, antibacterial, antiparasitic, antidiarrheal, antihypertensive, hypolipidemic, and fungicide.
AntiCan↑, elaborated on the anticancer effects of BBR through the regulation of different molecular pathways such as: inducing apoptosis, autophagy, arresting cell cycle, and inhibiting metastasis and invasion.
Apoptosis↑,
TumAuto↑,
TumCCA↑,
TumMeta↓,
TumCI↓,
eff↑, BBR is shown to have beneficial effects on cancer immunotherapy.
eff↑, BBR inhibited the release of Interleukin 1 beta (IL-1β), Interferon gamma (IFN-γ), Interleukin 6 (IL-6), and Tumor Necrosis Factor-alpha (TNF-α) from LPS stimulated lymphocytes by acting as a dopamine receptor antagonist
CD4+↓, BBR inhibited the proliferation of CD4+ T cells and down-regulated TNF-α and IL-1 and thus, improved autoimmune neuropathy.
TNF-α↓,
IL1↓,
BioAv↓, On the other hand, P-Glycoprotein (P-gp), a secretive pump located in the epithelial cell membrane, restricts the oral bioavailability of a variety of medications, such as BBR. The use of P-gp inhibitors is a common and effective way to prevent this
BioAv↓, Regardless of its low bioavailability, BBR has shown great therapeutic efficacy in the treatment of a number of diseases.
other↓, BBR has been also used as an effective therapeutic agent for Inflammatory Bowel Disease (IBD) for several years
AMPK↑, inhibitory effects on inflammation by regulating different mechanisms such as 5′ Adenosine Monophosphate-Activated Protein Kinase (AMPK. Increase of AMPK
MAPK↓, Mitogen-Activated Protein Kinase (MAPK), and NF-κB signaling pathways
NF-kB↓,
IL6↓, inhibiting the expression of proinflammatory genes such as IL-1, IL-6, Monocyte Chemoattractant Protein 1 (MCP1), TNF-α, Prostaglandin E2 (PGE2), and Cyclooxygenase-2 (COX-2)
MCP1/CCL2↓,
PGE2↓,
COX2/PTGS2↓,
*ROS↓, BBR protected PC-12 cells (normal) from oxidative damage by suppressing ROS through PI3K/AKT/mTOR signaling pathways
*antiOx↑, BBR therapy improved the antioxidant function of mice intestinal tissue by enhancing the levels of glutathione peroxidase and catalase enzymes.
*GPx↑,
*Catalase↑,
AntiTum↑, Besides, BBR leaves great antitumor effects on multiple types of cancer such as breast cancer,69 bladder cancer,70 hepatocarcinoma,71 and colon cancer.72
TumCP↓, BBR exerts its antitumor activity by inhibiting proliferation, inducing apoptosis and autophagy, and suppressing angiogenesis and metastasis
angioG↓,
Fas↑, by increasing the amounts of Fas receptor (death receptor)/FasL (Fas ligand), ROS, ATM, p53, Retinoblastoma protein (Rb), caspase-9,8,3, TNF-α, Bcl2-associated X protein (Bax), BID
FasL↑,
ROS↑,
ATM↑,
P53↑,
RB1↑,
Casp9↑,
Casp8↑,
Casp3↓,
BAX↑,
Bcl-2↓, and declining Bcl2, Bcl-X, c-IAP1 (inhibitor of apoptosis protein), X-linked inhibitor of apoptosis protein (XIAP), and Survivin levels
Bcl-xL↓,
IAP1↓,
XIAP↓,
survivin↓,
MMP2↓, Furthermore, BBR suppressed Matrix Metalloproteinase-2 (MMP-2), and MMP-9 expression.
MMP9↓,
CycB/CCNB1↓, Inhibition of cyclin B1, cdc2, cdc25c
CDC25↓,
CDC25↓,
Cyt‑c↑, BBR inhibited tumor cell proliferation and migration and induced mitochondria-mediated apoptosis pathway in Triple Negative Breast Cancer (TNBC) by: stimulating cytochrome c release from mitochondria to cytosol
MMP↓, decreased the mitochondrial membrane potential, and enabled cytochrome c release from mitochondria to cytosol
RenoP↑, BBR significantly reduced the destructive effects of cisplatin on the kidney by inhibiting autophagy, and exerted nephroprotective effects.
mTOR↓, U87 cell, Inhibition of m-TOR signaling
MDM2↓, Downregulation of MDM2
LC3II↑, Increase of LC3-II and beclin-1
ERK↓, BBR stimulated AMPK signaling, resulting in reduced extracellular signal–regulated kinase (ERK) activity and COX-2 expression in B16F-10 lung melanoma cells
COX2/PTGS2↓,
MMP3↓, reducing MMP-3 in SGC7901 GC and AGS cells
TGF-β↓, BBR suppressed the invasion and migration of prostate cancer PC-3 cells by inhibiting TGF-β-related signaling molecules which induced Epithelial-Mesenchymal Transition (EMT) such as Bone morphogenetic protein 7 (BMP7),
EMT↑,
ROCK1↓, inhibiting metastasis-associated proteins such as ROCK1, FAK, Ras Homolog Family Member A (RhoA), NF-κB and u-PA, leading to in vitro inhibition of MMP-1 and MMP-13.
FAK↓,
RAS↓,
Rho↓,
NF-kB↓,
uPA↓,
MMP1↓,
MMP13↓,
ChemoSen↑, recent studies have indicated that it can be used in combination with chemotherapy agents

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↑,

748- Bor,    A Study on the Anticarcinogenic Effects of Calcium Fructoborate
- in-vitro, BC, MDA-MB-231
p‑ATM↑,
p‑P53↑,
Casp9↑,
PARP↓, 2.5 fold decrease
VEGF↓,
Casp3↑, 50 μM CaFB only

7185- CHA,    Chaetocin-induced ROS-mediated apoptosis involves ATM–YAP1 axis and JNK-dependent inhibition of glucose metabolism
- vitro+vivo, GBM, A172 - in-vitro, GBM, T98G - in-vitro, GBM, U87MG
HMTs↓, Chaetocin, a histone methyltransferase inhibitor, is known to induce ROS generation.
ROS↑,
p‑ATM↑, Chaetocin-treated tumors exhibited heightened ROS, pATM, YAP1 and pJNK levels
YAP/TEAD↑, An increase in YAP1 level and decrease in YAP1 phosphorylation was observed upon Chaetocin treatment
p‑JNK↑,
TumPF↓, Chaetocin inhibits glioma cell proliferation
SUV39H↓, Chaetocin, an inhibitor of lysine-specific histone methyltransferase SUV39H1
TrxR↓, Chaetocin reduces thioredoxin reductase activity in a dose-dependent manner.
Casp3↑, Treatment with Chaetocin resulted in ∼3–5-fold increase in caspase-3 activity
Trx1↓, Chaetocin decreases the expression of TRX-1 in glioma cells
H3↓, Chaetocin-mediated inhibition of histone H3 methylation is ROS dependent
lactateProd↓, Chaetocin decreases lactate levels, ATP production and glucose uptake in a ROS- and JNK-dependent manner
ATP↓,
GlucoseCon↓,
TumCG↓, Chaetocin inhibits growth of tumor xenograft in nude mice
Dose↝, 10 animals each and were administered either with vehicle or Chaetocin (0.5 mg/kg body weight), intraperitoneally on alternate days for 25 days.

7167- CHA,    Chaetocin-induced ROS-mediated apoptosis involves ATM-YAP1 axis and JNK-dependent inhibition of glucose metabolism
- vitro+vivo, GBM, A172 - in-vitro, GBM, T98G - in-vitro, GBM, U87MG
HMTs↓, Chaetocin, a histone methyltransferase inhibitor, is known to induce ROS generation.
ROS↑,
YAP/TEAD↑, Increased intracellular ROS induced (i) Yes-associated protein 1 (YAP1) expression independent of the canonical Hippo pathway as well as (ii) ATM and JNK activation.
ATM↑,
JNK↑,
Apoptosis↑, Increased interaction of YAP1 with p73 and p300 induced apoptosis in an ATM-dependent manner.
GlucoseCon↓, decreased ATP production was accompanied by a ROS/JNK-dependent decrease in cellular glucose uptake by glioma cells in the presence of Chaetocin
lactateProd↓, A significant decrease in lactate production (Figure 5d) and ATP generation (Figure 5e) was observed in Chaetocin-treated cells as compared with the untreated control.
ATP↓,
TumCP↓, Chaetocin inhibits glioma cell proliferation
TrxR↓, Chaetocin treatment reduced thioredoxin reductase activity in a dose-dependent manner with ∼40% decrease in activity observed at 1 μM concentration
Trx1↓, Chaetocin decreases the expression of TRX-1 in glioma cells
H3K9↓, The decrease in H3K9me3 levels observed upon Chaetocin treatment was reverted in the presence of ROS inhibitor NAc
p‑ATM↑, Chaetocin induced an increase in pATM and γH2AX expression in a ROS-dependent manner
γH2AX↑,
ALDOB↑, ALDOB, ENO3, FBP1, FBP2 G6PC, GCK GSK3B, GYS2, HK3, PCK1, PGK2, PGM3, PHKG1, PKLR, PRPS1L1 and PYGM) were elevated by more than 2 fold upon Chaetocin treatment
ENO3↑,
FBP1↑,
GSK‐3β↑,
HK3↑,
PCK1↑,
PGK2↑,
PGM1↑,
PGM3↑,
PHKG1↑,
PKLR↑, PKLR, up-regulated by 20.9
HK2↓, HK2, downregulated by 4.5 fold
PCNA↓, Decrease in both PCNA-positive cells and its protein level in Chaetocin-treated tumors indicated inhibition of cell proliferation

1326- EMD,    Emodin induces a reactive oxygen species-dependent and ATM-p53-Bax mediated cytotoxicity in lung cancer cells
- in-vitro, Lung, A549
Apoptosis↑,
ROS↑,
P53↑,
BAX↑,
ATM↑,

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↑,

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/KDR/Flk1↓, Fisetin inhibited the VEGFR expression in Y79 cells as well as the angiogenesis of a tumor.
IAP2/BIRC3↓, 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

7048- GA,    Natural bioactive gallic acid shows potential anticancer effects by inhibiting the proliferation and invasiveness behavior in human embryonic carcinoma cells
- in-vitro, Var, NA
AntiCan↑, Natural gallic acid (GA) is noted to have anticancer properties for oncogene expression, cycle arrest, apoptosis, angiogenesis, migration and metastasis in various cancers.
TumCCA↑,
angioG↓,
TumCMig↓,
TumMeta↓,
CSCs↓, In two types of embryonic CSCs, GA effectively induced cell death via late apoptosis
Apoptosis↑,
P21↑, GA showed the G0/G1 cell cycle arrest activity in embryonic CSCs by inducing the increase of p21, p27 and p53 expression and the decrease of CDK4, cyclin E and cyclin D1 expression.
P53↑,
p27/CDKN1B↑,
CDK4↓,
cycE/CCNE↓,
cycD1/CCND1↓,
SOX2↓, GA inhibited the expression levels of mRNA and protein for stem cell markers, such as SOX2, NANOG and OCT4, in NTERA-2 and NCCIT cells.
Nanog↓,
OCT4↓,
ROS↑, The induction of cellular and mitochondrial reactive oxygen species by GA also activated the cellular DNA damage response pathway by raising the phosphorylated-BRCA1, ATM, Chk1, Chk2 and histone.
DNAdam↑,
BRCA1↑,
ATM↑,
CHK1↑,
Chk2↑,
Histones↑,
TumCI↓, GA inhibited CSCs invasion and migration by inhibiting the expression of matrix metalloproteinase by the downregulation of EGFR/JAK2/STAT5 signaling pathway.
MMPs↓,
EGFR↓,
JAK2↓,
STAT5↓,

487- MF,    Extremely Low-Frequency Electromagnetic Fields Cause G1 Phase Arrest through the Activation of the ATM-Chk2-p21 Pathway
- in-vitro, NMSC, HaCaT
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, NA
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.

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

5109- SSE,    Selenium compounds activate ATM-dependent DNA damage response via the mismatch repair protein hMLH1 in colorectal cancer cells
- in-vitro, CRC, HCT116
ROS↑, We show that hMLH1 complementation sensitizes HCT 116 cells to methylseleninic acid, methylselenocysteine, and sodium selenite via reactive oxygen species
DNAdam↓, and facilitates the selenium-induced oxidative 8-oxoguanine damage, DNA breaks, G2/M checkpoint response, and ATM pathway activation
ATM↑,
eff↓, Pretreatment of the hMLH1-complemented HCT 116 cells with the antioxidant N-acetylcysteine(NAC) or 2,2,6,6-tetramethylpiperidine-1-oxyl or the ATM kinase inhibitor KU55933 suppresses hMLH1-dependent DNA damage response to selenium exposure.
TumCCA↑, Selenium-induced cell cycle arrest and apoptosis in colon cancer cells has been well studied

2411- UA,    Ursolic acid in health and disease
- Review, Var, NA
Inflam↓, UA because of its beneficial effects, which include anti-inflammatory, anti-oxidant, anti-apoptotic, and anti-carcinogenic effects
antiOx↑,
NF-kB↓, Colon cancer HCT116, HT29 20 μM for 8 hour ↓ NF-kB, Bcl-xL, Bcl-2, and cyclin D1
Bcl-xL↓,
Bcl-2↓,
cycD1/CCND1↓,
Ki-67↓, ↓ Ki67, CD31, STAT3, and EGFR, ↑ p53 and p21 mRNA expression
CD31/PECAM-1↓,
STAT3↓,
EGFR↓,
P53↑,
P21↓,
HK2↓, MCF-7, MDA-MB-231 20 μM for 24 hours ↓ HK2, PKM2, ATP, and lactate ↓ pERK1/2, and depolarization of mitochondrial membrane potential, ↑ Nitric oxide and ATM
PKM2↓,
ATP↓,
lactateProd↓,
p‑ERK↓,
MMP↓,
NO↑,
ATM↑,
Casp3↑, T24 cancer cells ↑ Caspase 3 activity ↑ AMPK activation ↑ JNK activation
AMPK↑,
JNK↑,
FAO↑, 80 μM UA reduces triglyceride (TG) and cholesterol levels by increasing fatty acid oxidation and decreasing fatty acid synthesis in hepatocytes
FASN↓,
*GSH↑, ↑ Vitamin C, E, GSH, SOD, CAT, GPx, GST, and GR in heart
*SOD↑,
*Catalase↑,
*GPx↑,
*GSTs↑,
neuroP↑, This demonstrates that UA has a protective effect against various inflammatory conditions of the brain.


Showing Research Papers: 1 to 18 of 18

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 18

Pathway results for Effect on Cancer / Diseased Cells:


NA, unassigned(tgid=0) ⓘ

ALDOB↑, 1,   E2F4↑, 1,   ENO3↑, 1,   H3K9↓, 1,   HK3↑, 1,   PGK2↑, 1,   PGM3↑, 1,   PHKG1↑, 1,   PKLR↑, 1,   SUV39H↓, 1,   TRADD↑, 1,  

Redox & Oxidative Stress(tgid=1) ⓘ

antiOx↑, 1,   Ferroptosis↑, 1,   GSH↓, 1,   NRF2↑, 1,   ROS↑, 10,   mt-ROS↑, 1,   Trx1↓, 2,   TrxR↓, 2,  

Mitochondria & Bioenergetics(tgid=3) ⓘ

ATP↓, 3,   CDC2↓, 1,   CDC25↓, 3,   p‑CDC25↑, 1,   MMP↓, 4,   XIAP↓, 2,  

Core Metabolism/Glycolysis(tgid=4) ⓘ

AMPK↑, 2,   cMyc↓, 1,   FAO↑, 1,   FASN↓, 1,   FBP1↑, 1,   GlucoseCon↓, 2,   Histones↑, 2,   HK2↓, 2,   lactateProd↓, 3,   PCK1↓, 1,   PCK1↑, 1,   PGM1↑, 1,   PKM2↓, 1,  

Cell Death(tgid=5) ⓘ

Akt↓, 1,   Apoptosis↑, 8,   BAX↑, 4,   Bcl-2↓, 4,   Bcl-xL↓, 2,   Casp↑, 1,   Casp1↑, 1,   Casp2↑, 1,   Casp3↓, 1,   Casp3↑, 5,   Casp7↑, 1,   Casp8↑, 2,   Casp9↑, 4,   Chk2↑, 5,   p‑Chk2↑, 1,   CK2↓, 1,   Cyt‑c↑, 2,   Diablo↑, 1,   DR5↑, 1,   Fas↑, 3,   FasL↑, 1,   Ferroptosis↑, 1,   IAP1↓, 1,   IAP2/BIRC3↓, 1,   JNK↑, 2,   p‑JNK↑, 1,   MAPK↓, 2,   MDM2↓, 1,   oncosis↑, 1,   p27/CDKN1B↑, 3,   p‑p38↓, 1,   survivin↓, 3,   YAP/TEAD↑, 2,  

Transcription & Epigenetics(tgid=7) ⓘ

H3↓, 1,   p‑H3↓, 1,   other↓, 1,   tumCV↓, 1,  

Autophagy & Lysosomes(tgid=9) ⓘ

ATG5↑, 1,   Beclin-1↑, 1,   LC3II↑, 1,   LC3s↑, 1,   TumAuto↑, 2,  

DNA Damage & Repair(tgid=10) ⓘ

ATM↑, 13,   p‑ATM↑, 5,   ATR↑, 3,   p‑ATR↑, 1,   BRCA1↑, 1,   CHK1↑, 3,   p‑CHK1↑, 3,   DNAdam↓, 1,   DNAdam↑, 4,   HR↓, 1,   p16↑, 1,   P53↑, 8,   p‑P53↑, 1,   PARP↓, 1,   cl‑PARP↑, 1,   PCNA↓, 2,   RAD51↓, 1,   TP53↑, 1,   γH2AX↑, 2,  

Cell Cycle & Senescence(tgid=11) ⓘ

CDK2↓, 2,   CDK4↓, 4,   cycA1/CCNA1↑, 1,   CycB/CCNB1↓, 1,   cycD1/CCND1↓, 6,   cycE/CCNE↓, 2,   cycE1↓, 1,   P21↓, 1,   P21↑, 4,   RB1↑, 2,   TumCCA↑, 12,  

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

p‑cDC2↑, 1,   cMET↓, 1,   CSCs↓, 1,   EMT↑, 1,   ERK↓, 2,   p‑ERK↓, 1,   GSK‐3β↑, 2,   HMTs↓, 2,   mTOR↓, 2,   mTORC1↓, 1,   mTORC2↓, 1,   Nanog↓, 1,   OCT4↓, 1,   PI3K↓, 1,   RAS↓, 2,   SOX2↓, 1,   STAT3↓, 2,   STAT5↓, 1,   TumCG↓, 2,   Wnt/(β-catenin)↓, 1,  

Migration(tgid=13) ⓘ

Ca+2↑, 1,   CD31/PECAM-1↓, 1,   CDK4/6↓, 1,   E-cadherin↑, 1,   FAK↓, 1,   ITGB1↑, 1,   Ki-67↓, 2,   MMP1↓, 1,   MMP13↓, 2,   MMP2↓, 2,   MMP3↓, 1,   MMP7↓, 1,   MMP9↓, 1,   MMPs↓, 2,   NCAM↑, 1,   Rho↓, 2,   ROCK1↓, 1,   TGF-β↓, 2,   TIMP2↑, 1,   TumCI↓, 2,   TumCMig↓, 2,   TumCP↓, 4,   TumMeta↓, 2,   TumPF↓, 1,   uPA↓, 2,  

Angiogenesis & Vasculature(tgid=14) ⓘ

angioG↓, 3,   EGFR↓, 3,   Hif1a↓, 1,   NO↓, 1,   NO↑, 2,   VEGF↓, 3,   VEGFR2/KDR/Flk1↓, 2,  

Immune & Inflammatory Signaling(tgid=16) ⓘ

CD4+↓, 1,   cellSen↑, 1,   COX2/PTGS2↓, 2,   CXCR2↑, 1,   IL1↓, 2,   IL6↓, 2,   Inflam↓, 2,   JAK1↓, 1,   JAK2↓, 1,   MCP1/CCL2↓, 1,   MIP2↓, 1,   NF-kB↓, 5,   PGE2↓, 2,   TNF-α↓, 3,  

Hormonal & Nuclear Receptors(tgid=20) ⓘ

CDK6↓, 2,  

Drug Metabolism & Resistance(tgid=21) ⓘ

BioAv↓, 2,   ChemoSen↑, 2,   Dose↝, 3,   eff↓, 3,   eff↑, 2,   Half-Life↓, 1,  

Clinical Biomarkers(tgid=22) ⓘ

BRCA1↑, 1,   EGFR↓, 3,   IL6↓, 2,   Ki-67↓, 2,   TP53↑, 1,  

Functional Outcomes(tgid=23) ⓘ

AntiCan↑, 2,   AntiTum↑, 1,   chemoP↑, 1,   hepatoP↑, 1,   neuroP↑, 2,   RenoP↑, 2,  
Total Targets: 194

Pathway results for Effect on Normal Cells:


Redox & Oxidative Stress(tgid=1) ⓘ

antiOx↑, 2,   Catalase↑, 2,   GPx↑, 2,   GSH↑, 1,   GSTs↑, 1,   ROS↓, 2,   SIRT3↑, 1,   SOD↑, 1,  

Core Metabolism/Glycolysis(tgid=4) ⓘ

SIRT1↑, 1,  

Cell Death(tgid=5) ⓘ

Apoptosis↓, 1,  

DNA Damage & Repair(tgid=10) ⓘ

ATM↑, 1,  

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

CD34↑, 1,   FOXO1↑, 1,   FOXO3↑, 1,  

Angiogenesis & Vasculature(tgid=14) ⓘ

Hif1a↑, 1,  

Immune & Inflammatory Signaling(tgid=16) ⓘ

Inflam↓, 1,  
Total Targets: 16

Scientific Paper Hit Count for: ATM, similar to Serine-protein kinase ATM (Ataxia telangiectasia mutated) (A-T, mutated); ataxia telangiectasia mutated
2 chaetocin
2 Ferulic acid
1 Alpha-Lipoic-Acid
1 Apigenin (mainly Parsley)
1 Artemisinin
1 Berberine
1 borneol
1 Cisplatin
1 Boron
1 Emodin
1 Fisetin
1 Gallic acid
1 Magnetic Fields
1 Phenethyl isothiocyanate
1 Resveratrol
1 Selenite (Sodium)
1 Ursolic 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#:20  State#:%  Dir#:2
  wNotes=on  sortOrder:rid,rpid

 

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