HATs Cancer Research Results
HATs, histone acetyltransferases: Click to Expand ⟱
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Histone acetyltransferases (HATs) are a family of enzymes that play a crucial role in the regulation of gene expression by modifying chromatin structure. HATs transfer acetyl groups to the lysine residues of histone proteins, which are the main components of chromatin. This modification, known as histone acetylation, leads to the relaxation of chromatin structure, allowing for increased access of transcription factors to DNA and promoting gene expression.
HATs is overexpressed in cancers with poor prognosis.
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Scientific Papers found: Click to Expand⟱
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in-vitro, |
Cerv, |
HeLa |
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in-vitro, |
Cerv, |
SiHa |
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in-vitro, |
Cerv, |
C33A |
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DNMTs↓, ALA increased DNA demethylase, HMTs, and HATs while decreasing global DNA methylation, DNMT, HDMs, and HDACs mRNA expression/activity in all cervical cancer cell lines.
HDAC↓,
HATs↑,
hTERT/TERT↓, ALA downregulated hTERT oncogene while upregulating the mRNA expression of TSGs (Tumor Suppressor Genes) CDH1, RARβ, and DAPK in all the cell lines.
CDH1↑,
RARβ↑,
DNMT1↓, In HeLa, ALA treatment reduced DNMT1 mRNA expression by 2.3-fold, 2.9-fold, and 3.3-fold at 20, 40, and 80 μM, respectively,
DNMT3A↓, ALA also reduced DNMT3B mRNA expression: in HeLa by 3.5-fold and 3.2-fold at 40 and 80 μM, i
TET2↑, ALA treatment induced TET2 mRNA expression, with an increase of 3.6-fold in HeLa at 80 μM.
HDAC1↓, ALA treatment in HeLa resulted in a significant reduction in HDAC1 mRNA expression, with decreases of 2.3-fold and 3.8-fold at 40 and 80 μM,
HDAC8↓, Treatment with ALA at 80 μM also led to reductions in HDAC8 mRNA expression by 2.4-fold, 2.0-fold, and 2.0-fold in HeLa, SiHa, and C33A, respectively.
SIRT1↓, ALA additionally decreased SIRT1 mRNA expression in HeLa by 2.4-fold and 2.5-fold at 40 and 80 μM, respectively.
HMTs↑,
EZH2↓, In HeLa, ALA treatment decreased EZH2 mRNA expression by 2.9-fold, 4.2-fold, and 4.2-fold at 20, 40, and 80 µM, respectively.
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in-vitro, |
CRC, |
HCT116 |
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in-vitro, |
CRC, |
HT29 |
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HDAC↓, butyrate accumulated and functioned as an HDAC inhibitor.
Warburg↓, Consequently, butyrate stimulated the proliferation of normal colonocytes and cancerous colonocytes when the Warburg effect was prevented from occurring, whereas it inhibited the proliferation of cancerous colonocytes undergoing the Warburg effect.
TumCP⇅, Butyrate Increases or Decreases Cell Proliferation Depending on the Warburg Effect
HATs↑, Butyrate Induces Histone Acetylation by Stimulating HATs as well as Inhibiting HDACs
BioAv↓, However, the efficacy of butyrate as a chemotherapeutic agent has been limited by its rapid uptake and metabolism by normal cells [resulting in a half-life of 6 minutes and peak blood levels below 0.05 mM (Miller et al., 1987)] before reaching tumors
other↝, A fiber-rich diet might be more successful for chemoprevention because it delivers mM levels of butyrate (via the microbiota) to the correct place (the colon) before the onset of tumorigenesis or at an early stage.
Risk↓, Evidence for this idea comes from recent human studies demonstrating lower levels of butyrate-producing bacteria among the gut microbiota of colorectal cancer patients compared to healthy participants
TumCCA↑, induction of G0/G1 and G2/M cell cycle arrest
CDK2↓, (via the regulation of cyclin-dependent kinase (CDK) and cyclin proteins),
EMT↓, epithelial–mesenchymal transition inhibition via the downregulation of mesenchymal markers
MMPs↓, honokiol possesses the capability to supress cell migration and invasion via the downregulation of several matrix-metalloproteinases
AMPK↑, (activation of 5′ AMP-activated protein kinase (AMPK) and KISS1/KISS1R signalling)
TumCI↓, inhibiting cell migration, invasion, and metastasis, as well as inducing anti-angiogenesis activity (via the down-regulation of vascular endothelial growth factor (VEGFR) and vascular endothelial growth factor (VEGF)
TumCMig↓,
TumMeta↓,
VEGFR2↓,
*antiOx↑, diverse biological activities, including anti-arrhythmic, anti-inflammatory, anti-oxidative, anti-depressant, anti-thrombocytic, and anxiolytic activities
*Inflam↓,
*BBB↑, Due to its ability to cross the blood–brain barrier
*neuroP↑, beneficial towards neuronal protection through various mechanism, such as the preservation of Na+/K+ ATPase, phosphorylation of pro-survival factors, preservation of mitochondria, prevention of glucose, reactive oxgen species (ROS), and inflammatory
*ROS↓,
Dose↝, Generally, the concentrations used for the in vitro studies are between 0–150 μM
selectivity↑, Interestingly, honokiol has been shown to exhibit minimal cytotoxicity against on normal cell lines, including human fibroblast FB-1, FB-2, Hs68, and NIH-3T3 cells
Casp3↑, ↑ Caspase-3 & caspase-9
Casp9↑,
NOTCH1↓, Inhibition of Notch signalling: ↓ Notch1 & Jagged-1;
cycD1/CCND1↓, ↓ cyclin D1 & c-Myc;
cMyc↓,
P21?, ↑ p21WAF1 protein
DR5↑, ↑ DR5 & cleaved PARP
cl‑PARP↑,
P53↑, ↑ phosphorylated p53 & p53
Mcl-1↑, ↓ Mcl-1 protein
p65↓, ↓ p65; ↓ NF-κB
NF-kB↓,
ROS↑, ↑ JNK activation ,Increase ROS activity:
JNK↑,
NRF2↑, ↑ Nrf2 & c-Jun protein activation
cJun↑,
EF-1α↓, ↓ EFGR; ↓ MAPK/PI3K pathway activity
MAPK↓,
PI3K↓,
mTORC1↓, ↓ mTORC1 function; ↑ LKB1 & cytosolic localisation
CSCs↓, Inhibit stem-like characteristics: ↓ Oct4, Nanog & Sox4 protein; ↓ STAT3;
OCT4↓,
Nanog↓,
SOX4↓,
STAT3↓,
CDK4↓, ↓ Cdk2, Cdk4 & p-pRbSer780;
p‑RB1↓,
PGE2↓, ↓ PGE2 production ↓ COX-2 ↑ β-catenin
COX2↓,
β-catenin/ZEB1↑,
IKKα↓, ↓ IKKα
HDAC↓, ↓ class I HDAC proteins; ↓ HDAC activity;
HATs↑, ↑ histone acetyltransferase (HAT) activity; ↑ histone H3 & H4
H3↑,
H4↑,
LC3II↑, ↑ LC3-II
c-Raf↓, ↓ c-RAF
SIRT3↑, ↑ Sirt3 mRNA & protein; ↓ Hif-1α protein
Hif1a↓,
ER Stress↑, ↑ ER stress signalling pathway activation; ↑ GRP78,
GRP78/BiP↑,
cl‑CHOP↑, ↑ cleaved caspase-9 & CHOP;
MMP↓, mitochondrial depolarization
PCNA↓, ↓ cyclin B1, cyclin D1, cyclin D2 & PCNA;
Zeb1↓, ↓ ZEB2
Inhibit
NOTCH3↓, ↓ Notch3/Hes1 pathway
CD133↓, ↓ CD133 & Nestin protein
Nestin↓,
ATG5↑, ↑ Atg7 protein activation; ↑ Atg5;
ATG7↑,
survivin↓, ↓ Mcl-1 & survivin protein
ChemoSen↑, honokiol potentiated the apoptotic effect of both doxorubicin and paclitaxel against human liver cancer HepG2 cells.
SOX2↓, Honokiol was shown to downregulate the expression of Oct4, Nanog, and Sox2 which were known to be expressed in osteosarcoma, breast carcinoma and germ cell tumours
OS↑, Lipo-HNK was also shown to prolong survival and induce intra-tumoral apoptosis in vivo.
P-gp↓, Honokiol was shown to downregulate the expression of P-gp at mRNA and protein levels in MCF-7/ADR, a human breast MDR cancer cell line
Half-Life↓, For i.v. administration, it has been found that there was a rapid rate of distribution followed by a slower rate of elimination (elimination half-life t1/2 = 49.22 min and 56.2 min for 5 mg or 10 mg of honokiol, respectively
Half-Life↝, male and female dogs was assessed. The elimination half-life (t1/2 in hours) was found to be 20.13 (female), 9.27 (female), 7.06 (male), 4.70 (male), and 1.89 (male) after administration of doses of 8.8, 19.8, 3.9, 44.4, and 66.7 mg/kg, respectively.
eff↑, Apart from that, epigallocatechin-3-gallate functionalized chitin loaded with honokiol nanoparticles (CE-HK NP), developed by Tang et al. [224], inhibit HepG2
BioAv↓, extensive biotransformation of honokiol may contribute to its low bioavailability.
HDAC↓, Other HDACIs include the aliphatic acids, such as phenylbutyrate and its derivatives valproic acid and MS-275, which are in phase I and II clinical trials
HATs↑, The primary role of HDACs is to oppose the activity of histone acetyltransferases (HATs) balancing the level of acetylation of the histones.
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in-vitro, |
Lung, |
A549 |
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in-vitro, |
Lung, |
H1299 |
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in-vitro, |
Lung, |
H460 |
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HDAC↓, associated with the inhibition of histone deacetylase (HDAC) activity and reduced levels of class 1 HDAC proteins (HDAC1, HDAC2, HDAC3 and HDAC8
HDAC1↓,
HDAC2↓,
HDAC3↓,
HDAC8↓,
HATs↑, and concomitant increases in the levels of histone acetyltransferase activity (HAT).
Zeb1↓, Treatment of A549 and H460 cells with silymarin reduced the expression of the transcription factor ZEB1 and restored expression of E-cadherin.
E-cadherin↑,
TumCMig↓, These findings indicate that silymarin can effectively inhibit lung cancer cell migration
Inflam↓, Silymarin, a milk thistle extract, has anti-inflammatory, immunomodulatory, anti-lipid peroxidative, anti-fibrotic, anti-oxidative, and anti-proliferative properties.
lipid-P↓,
TumMeta↓, Silymarin exhibits not only anti-cancer functions through modulating various hallmarks of cancer, including cell cycle, metastasis, angiogenesis, apoptosis, and autophagy, by targeting a plethora of molecules
angioG↓,
chemoP↑, but also plays protective roles against chemotherapy-induced toxicity, such as nephrotoxicity,
EMT↓, Figure 2, Metastasis
HDAC↓,
HATs↑,
MMPs↓,
uPA↓,
PI3K↓,
Akt↓,
VEGF↓, Angiogenesis
CD31↓,
Hif1a↓,
VEGFR2↓,
Raf↓,
MEK↓,
ERK↓,
BIM↓, apoptosis
BAX↑,
Bcl-2↓,
Bcl-xL↓,
Casp↑,
MAPK↓,
P53↑,
LC3II↑, Autophagy
mTOR↓,
YAP/TEAD↓,
*BioAv↓, Additionally, the oral bioavailability of silymarin in rats is only 0.73 %
MMP↓, silymarin treatment reduced mitochondrial transmembrane potential, leading to an increase in cytosolic cytochrome c (Cyt c), downregulating proliferation-associated proteins (PCNA, c-Myc, cyclin D1, and β-catenin)
Cyt‑c↑,
PCNA↓,
cMyc↓,
cycD1/CCND1↓,
β-catenin/ZEB1↓,
survivin↓, and anti-apoptotic proteins (survivin and Bcl-2), and upregulating pro-apoptotic proteins (caspase-3, Bax, APAF-1, and p53)
APAF1↑,
Casp3↑,
MDSCs↓, ↓MDSCs, ↓IL-10, ↑IL-2 and IFN-γ
IL10↓,
IL2↑,
IFN-γ↑,
hepatoP↑, Moreover, in a randomized clinical trial, silymarin attenuated hepatoxicity in non-metastatic breast cancer patients undergoing a doxorubicin/cyclophosphamide-paclitaxel regimen
cardioP↑, For example, Rašković et al. studied the hepatoprotective and cardioprotective effects of silymarin (60 mg/kg orally) in rats following DOX
GSH↑, silymarin could protect the kidney and heart from ADR toxicity by protecting against glutathione (GSH) depletion and inhibiting lipid peroxidation
neuroP↑, silymarin attenuated the neurotoxicity of docetaxel by reducing apoptosis, inflammation, and oxidative stress
hepatoP↑, This group of flavonoids has been extensively studied and they have been used as hepato-protective substances
AntiCan↑, however, silymarin compounds have clear anticancer effects
TumCMig↓, decreasing migration through multiple targeting, decreasing hypoxia inducible factor-1α expression, i
Hif1a↓, In prostate cancer cells silibinin inhibited HIF-1α translation
selectivity↑, antitumoral activity of silymarin compounds is limited to malignant cells while the nonmalignant cells seem not to be affected
toxicity∅, long history of silymarin use in human diseases without toxicity after prolonged administration.
*antiOx↑, as an antioxidant, by scavenging prooxidant free radicals
*Inflam↓, antiinflammatory effects similar to those of indomethacin,
TumCCA↑, MDA-MB 486 breast cancer cells, G1 arrest was found due to increased p21 and decreased CDKs activity
P21↑,
CDK4↓,
NF-kB↓, human prostate carcinoma cells, silymarin decreased ligand binding to Erb1 135 and NF-kB expression was strongly inhibited by silymarin in hepatoma cell
ERK↓, human prostate carcinoma cells, silymarin decreased ligand binding to Erb1 135 and NF-kB expression was strongly inhibited by silymarin in hepatoma cell
PSA↓, Treating prostate carcinoma cells with silymarin the levels of PSA were significantly decreased and cell growth was inhibited through decreased CDK activity and induction of Cip1/p21 and Kip1/p27. 1
TumCG↓,
p27↑,
COX2↓, such as anti-COX2 and anti-IL-1α activity, 140 antiangiogenic effects through inhibition of VEGF secretion, upregulation of Insulin like Growth Factor Binding Protein 3 (IGFBP3), 141 and inhibition of androgen receptors.
IL1↓,
VEGF↓,
IGFBP3↑,
AR↓,
STAT3↓, downregulation of the STAT3 pathway which was seen in many cell models.
Telomerase↓, silymarin has the ability to decrease telomerase activity in prostate cancer cells
Cyt‑c↑, mitochondrial cytochrome C release-caspase activation.
Casp↑,
eff↝, Malignant p53 negative cells show only minimal apoptosis when treated with silymarin. Therefore, one conclusion is that silymarin may be useful in tumors with conserved p53.
HDAC↓, inhibit histone deacetylase activity;
HATs↑, increase histone acetyltransferase activity
Zeb1↓, reduce expression of the transcription factor ZEB1
E-cadherin↑, increase expression of E-cadherin;
miR-203↑, increase expression of miR-203
NHE1↓, reduce activation of sodium hydrogen isoform 1 exchanger (NHE1)
MMP2↓, target β catenin and reduce the levels of MMP2 and MMP9
MMP9↓,
PGE2↓, reduce activation of prostaglandin E2
Vim↓, suppress vimentin expression
Wnt↓, inhibit Wnt signaling
angioG↓, Silymarin inhibits angiogenesis.
VEGF↓, VEGF downregulation
*TIMP1↓, Silymarin has the capacity to decrease TIMP1 expression166–168 in mice.
EMT↓, found that silibinin had no effect on EMT. However, the opposite was found in other malignant tissues160–162 where it showed inhibitory effects.
TGF-β↓, Silibinin reduces the expression of TGF β2 in different tumors such as triple negative breast, 174 prostate, and colorectal cancers.
CD44↓, Silibinin decreased CD44 expression and the activation of EGFR (epidermal growth factor receptor)
EGFR↓,
PDGF↓, silibinin had the ability to downregulate PDFG in fibroblasts, thus decreasing proliferation.
*IL8↓, Flavonoids, in general, reduce levels of IL-8. Curcumin, 200 apigenin, 201 and silybin showed the ability to decrease IL-8 levels
SREBP1↓, Silymarin inhibited STAT3 phosphorylation and decreased the expression of intranuclear sterol regulatory element binding protein 1 (SREBP1), decreasing lipid synthesis.
MMP↓, reduced membrane potential and ATP content
ATP↓,
uPA↓, silibinin decreased MMP2, MMP9, and urokinase plasminogen activator receptor level (uPAR) in neuroblastoma cells. uPAR is also a marker of cell invasion.
PD-L1↓, Silibinin inhibits PD-L1 by impeding STAT5 binding in NSCLC.
NOTCH↓, Silybin inhibited Notch signaling in hepatocellular carcinoma cells showing antitumoral effects
*SIRT1↑, Silymarin can also increase SIRT1 expression in other tissues, such as hippocampus, 221 articular chondrocytes, 222 and heart muscle
SIRT1↓, Silymarin seems to act differently in tumors: in lung cancer cells SIRT downregulated SIRT1 and exerted multiple antitumor effects such as reduced adhesion and migration and increased apoptosis.
CA↓, Silymarin has the ability to inhibit CA isoforms CA I and CA II.
Ca+2↑, ilymarin increases mitochondrial release of Ca++ and lowers mitochondrial membrane potential in cancer cell
chemoP↑, Silymarin: Decreasing Side Effects and Toxicity of Chemotherapeutic Drugs
cardioP↑, There is also evidence that it protects the heart from doxorubicin toxicity, however, it is less potent than quercetin in this effect.
Dose↝, oral administration of 240 mg of silybin to 6 healthy volunteers the following results were obtained 377 : maximum\,plasmaconcentration0.34±0.16𝜇g/mL
Half-Life↝, and time to maximum plasma concentration 1.32 ± 0.45 h. Absorption half life 0.17 ± 0.09 h, elimination half life 6.32 ± 3.94 h
BioAv↓, silymarin is not soluble in water and oral administration shows poor absorption in the alimentary tract (approximately 1% in rats,
BioAv↓, Our conclusion is that, from a bioavailability standpoint, it is much easier to achieve migration inhibition, than proliferative reduction.
BioAv↓, Combination with succinate: is available on the market under the trade mark Legalon® (bis hemisuccinate silybin). Combination with phosphatidylcholine:
toxicity↝, 13 g daily per os divided into 3 doses was well tolerated. The most frequent adverse event was asymptomatic liver toxicity.
Half-Life↓, It may be necessary to administer 800 mg 4 times a day because the half-life is short.
ROS↓, its ability as an antioxidant reduces ROS production
FAK↓, Silibinin decreased human osteosarcoma cell invasion through Erk inhibition of a FAK/ERK/uPA/MMP2 pathway
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 ⓘ
GSH↑, 1, lipid-P↓, 1, NRF2↑, 1, ROS↓, 1, ROS↑, 1, SIRT3↑, 1,
Mitochondria & Bioenergetics ⓘ
ATP↓, 1, MEK↓, 1, MMP↓, 3, Raf↓, 1, c-Raf↓, 1,
Core Metabolism/Glycolysis ⓘ
AMPK↑, 1, ATG7↑, 1, cMyc↓, 2, RARβ↑, 1, SIRT1↓, 2, SREBP1↓, 1, Warburg↓, 1,
Cell Death ⓘ
Akt↓, 1, APAF1↑, 1, BAX↑, 1, Bcl-2↓, 1, Bcl-xL↓, 1, BIM↓, 1, Casp↑, 2, Casp3↑, 2, Casp9↑, 1, Cyt‑c↑, 2, DR5↑, 1, hTERT/TERT↓, 1, JNK↑, 1, MAPK↓, 2, Mcl-1↑, 1, p27↑, 1, survivin↓, 2, Telomerase↓, 1, YAP/TEAD↓, 1,
Kinase & Signal Transduction ⓘ
EF-1α↓, 1,
Transcription & Epigenetics ⓘ
cJun↑, 1, EZH2↓, 1, H3↑, 1, H4↑, 1, HATs↑, 7, other↝, 1,
Protein Folding & ER Stress ⓘ
cl‑CHOP↑, 1, ER Stress↑, 1, GRP78/BiP↑, 1,
Autophagy & Lysosomes ⓘ
ATG5↑, 1, LC3II↑, 2,
DNA Damage & Repair ⓘ
DNMT1↓, 1, DNMT3A↓, 1, DNMTs↓, 1, P53↑, 2, cl‑PARP↑, 1, PCNA↓, 2,
Cell Cycle & Senescence ⓘ
CDK2↓, 1, CDK4↓, 2, cycD1/CCND1↓, 2, P21?, 1, P21↑, 1, p‑RB1↓, 1, TumCCA↑, 2,
Proliferation, Differentiation & Cell State ⓘ
CD133↓, 1, CD44↓, 1, CSCs↓, 1, EMT↓, 3, ERK↓, 2, HDAC↓, 7, HDAC1↓, 2, HDAC2↓, 1, HDAC3↓, 1, HDAC8↓, 2, HMTs↑, 1, IGFBP3↑, 1, mTOR↓, 1, mTORC1↓, 1, Nanog↓, 1, Nestin↓, 1, NOTCH↓, 1, NOTCH1↓, 1, NOTCH3↓, 1, OCT4↓, 1, PI3K↓, 2, SOX2↓, 1, STAT3↓, 2, TumCG↓, 1, Wnt↓, 1,
Migration ⓘ
CA↓, 1, Ca+2↑, 1, CD31↓, 1, CDH1↑, 1, E-cadherin↑, 2, FAK↓, 1, miR-203↑, 1, MMP2↓, 1, MMP9↓, 1, MMPs↓, 2, PDGF↓, 1, SOX4↓, 1, TGF-β↓, 1, TumCI↓, 1, TumCMig↓, 3, TumCP⇅, 1, TumMeta↓, 2, uPA↓, 2, Vim↓, 1, Zeb1↓, 3, β-catenin/ZEB1↓, 1, β-catenin/ZEB1↑, 1,
Angiogenesis & Vasculature ⓘ
angioG↓, 2, EGFR↓, 1, Hif1a↓, 3, VEGF↓, 3, VEGFR2↓, 2,
Barriers & Transport ⓘ
NHE1↓, 1, P-gp↓, 1,
Immune & Inflammatory Signaling ⓘ
COX2↓, 2, IFN-γ↑, 1, IKKα↓, 1, IL1↓, 1, IL10↓, 1, IL2↑, 1, Inflam↓, 1, MDSCs↓, 1, NF-kB↓, 2, p65↓, 1, PD-L1↓, 1, PGE2↓, 2, PSA↓, 1,
Hormonal & Nuclear Receptors ⓘ
AR↓, 1,
Drug Metabolism & Resistance ⓘ
BioAv↓, 5, ChemoSen↑, 1, Dose↝, 2, eff↑, 1, eff↝, 1, Half-Life↓, 2, Half-Life↝, 2, selectivity↑, 2, TET2↑, 1,
Clinical Biomarkers ⓘ
AR↓, 1, EGFR↓, 1, EZH2↓, 1, hTERT/TERT↓, 1, PD-L1↓, 1, PSA↓, 1,
Functional Outcomes ⓘ
AntiCan↑, 1, cardioP↑, 2, chemoP↑, 2, hepatoP↑, 2, neuroP↑, 1, OS↑, 1, Risk↓, 1, toxicity↝, 1, toxicity∅, 1,
Total Targets: 154
Pathway results for Effect on Normal Cells:
Redox & Oxidative Stress ⓘ
antiOx↑, 2, ROS↓, 1,
Core Metabolism/Glycolysis ⓘ
SIRT1↑, 1,
Migration ⓘ
TIMP1↓, 1,
Barriers & Transport ⓘ
BBB↑, 1,
Immune & Inflammatory Signaling ⓘ
IL8↓, 1, Inflam↓, 2,
Drug Metabolism & Resistance ⓘ
BioAv↓, 1,
Functional Outcomes ⓘ
neuroP↑, 1,
Total Targets: 9
Scientific Paper Hit Count for: HATs, histone acetyltransferases
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#:886 State#:% Dir#:2
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