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.
Scientific Papers found: Click to Expand⟱
1078- And,    Andrographolide inhibits breast cancer through suppressing COX-2 expression and angiogenesis via inactivation of p300 signaling and VEGF pathway
- in-vitro, BC, MDA-MB-231 - in-vitro, Nor, HUVECs - in-vivo, BC, MCF-7 - in-vitro, BC, T47D - in-vitro, BC, BT549 - in-vitro, BC, MDA-MB-361
TumCP↓,
COX2↓, suppress COX-2 expression at both protein and mRNA levels.
*angioG↓,
Cyt‑c↑,
CREB2↓, inhibited the binding of the transactivators CREB2, C-Fos and NF-κB
cFos↓,
NF-kB↓,
HATs↓,
cl‑Casp3↑,
cl‑Casp9↑,
Bax:Bcl2↑,
Apoptosis↑,
*toxicity↓, IC50: 50uM for normal vs 20-35uM for cancer cells

5793- ASA,    Aspirin Recapitulates Features of Caloric Restriction
- in-vitro, Nor, NA
*CRM↑, Altogether, these findings identify aspirin as an evolutionary conserved CRM.
*HATs↓, inhibit the acetyltransferase activity of EP300
*NF-kB↓, aspirin reportedly inhibits the activation of the pro-inflammatory transcription factor nuclear factor kappa light-chain enhancer of activated B cell (NF-κB)
*EP300↓, Salicylate Inhibits EP300 Acetyltransferase by Competing with AcCoA

1505- CUR,    Epigenetic targets of bioactive dietary components for cancer prevention and therapy
- Review, NA, NA
TumCCA↑,
Apoptosis↑,
DNMTs↓, curcumin also inhibits DNMT activities and histone modification such as HDAC inhibition in tumorigenesis
HDAC↓,
HATs↓, inhibitory activity against HDACs and HATs in several in vitro cancer models
TumCP↓,
p300↓, Significant decreases in the amounts of p300, HDAC1, HDAC3, and HDAC8
HDAC1↓,
HDAC3↓,
HDAC8↓,
NF-kB↓, inhibition of nuclear translocation of the NF-κB/p65 subunit

2816- CUR,    NEUROPROTECTIVE EFFECTS OF CURCUMIN
- Review, AD, NA - Review, Park, NA
*neuroP↑, Curcumin has an outstanding safety profile and a number of pleiotropic actions with potential for neuroprotective efficacy, including anti-inflammatory, antioxidant, and anti-protein-aggregate activities.
*Inflam↓,
*antiOx↑,
*BioAv↓, despite concerns about poor oral bioavailability, curcumin has at least 10 known neuroprotective action
*AP-1↓, Curcumin inhibition of AP-1 and NF-κB-mediated transcription occurs at relatively low (<100 nM) doses and might be due to inhibition of histone acetylase (HAT) or activation of histone deacetylase (HDAC) activity
*NF-kB↓,
*HATs↓,
*HDAC↑,
Dose↑, At high doses (>3 µM) that are relevant to colon cancer but unlikely achievable with oral delivery in plasma and tissues outside of the gut, curcumin can act as an alkylating agent,10 a phase II enzyme inducer,11 and stimulate antioxidant response el
*ROS↓, We also found that curcmin reduced oxidative damage, inflammation, and cognitive deficits in rats receiving CNS infusions of toxic Aβ
*cognitive↑,
*Aβ↓, dose-dependently blocked Aβ aggregation at submicromolar concentrations

3238- EGCG,    Green tea catechin, epigallocatechin-3-gallate (EGCG): mechanisms, perspectives and clinical applications
- Review, Var, NA
Telomerase↓, EGCG stimulates telomere fragmentation through inhibiting telomerase activity.
DNMTs↓, EGCG reduced DNMTs,
cycD1/CCND1↓, EGCG also reduced the protein expression of cyclin D1, cyclin E, CDK2, CDK4, and CDK6. EGCG also inhibited the activity of CDK2 and CDK4, and caused Rb hypophosphorylation
cycE/CCNE↓,
CDK2↓,
CDK4↓,
CDK6↓,
HATs↓, EGCG can inhibit certain biomedically important molecular targets such as DNMTs, HATs, and HDACs
HDAC↓,
selectivity↑, EGCG has shown higher cytotoxicity in cancer cells than in their normal counterparts.
uPA↓, EGCG blocks urokinase, an enzyme which is essential for cancer growth and metastasis
NF-kB↓, EGCG inhibits NFκB and expression of TNF-α, reduces cancer promotion
TNF-α↓,
*ROS↓, It acts as strong ROS scavenger and antioxidant,
*antiOx↑,
Hif1a↓, ↓ HIF-1α; ↓ VEGF; ↓ VEGFR1;
VEGF↓,
MMP2↓, ↓ MMP-2; ↓ MMP-9; ↓ FAK;
MMP9↓,
FAK↓,
TIMP2↑, TIMP-2; ↑
Mcl-1↓, ↓ Mcl-1; ↓ survivin; ↓ XIAP
survivin↓,
XIAP↓,
PCNA↓, ↓ PCNA; ↑ 16; ↑ p18; ↑ p21; ↑ p27; ↑ pRb; ↑ p53; ↑ mdm2
p16↑,
P21↑,
p27↑,
pRB↑,
P53↑,
MDM2↑,
ROS↑, ↑ ROS; ↑ caspase-3; ↑ caspase-8; ↑ caspase-9; ↑ cytochrome c; ↑ Smac/DIABLO; ↓↑ Bax; Z Bak; ↓ cleaved PPAR;
Casp3↑,
Casp8↑,
Casp9↑,
Cyt‑c↑,
Diablo↑,
BAX⇅,
cl‑PPARα↓,
PDGF↓, ↓ PDGF; ↓ PDGFRb; ↓ EGFR;
EGFR↓,
FOXO↑, activated FOXO transcription factors
AP-1↓, The inhibition of AP-1 activity by EGCG was associated with inhibition of JNK activation but not ERK activation.
JNK↓,
COX2↓, EGCG reduces the activity of COX-2 following interleukin-1A stimulation of human chondrocytes
angioG↓, EGCG inhibits angiogenesis by enhancing FOXO transcriptional activity

1503- EGCG,    Epigenetic targets of bioactive dietary components for cancer prevention and therapy
- Review, NA, NA
selectivity↑, EGCG has been shown to induce apoptosis and cell cycle arrest in many cancer cells without affecting normal cells
DNMT1↓, inhibition of DNMT1 leading to demethylation and reactivation of methylation-silenced genes.
RECK↑, EGCG-induced epigenetic reactivation of RECK
MMPs↓, negatively regulates matrix metalloproteinases (MMPs)
TumCI↓, inhibits tumor invasion, angiogenesis, and metastasis
angioG↓,
TumMeta↓,
HATs↓, EGCG has strong HAT inhibitory activity
IκB↑, increases the level of cytosolic IκBα
NF-kB↓, suppresses tumor necrosis factor α-induced NF-κB activation
IL6↓,
COX2↓,
NOS2↓,
ac‑H3↑, increased the levels of acetylated histone H3 (LysH9/18) and H4 levels
ac‑H4↑,
eff↑, EGCG may synergize with the HDAC inhibitory action of vorinostat to help de-repress silenced tumor suppressor genes regulating key functions such as proliferation and cell survival

805- GAR,  Cisplatin,  PacT,    Garcinol Exhibits Anti-Neoplastic Effects by Targeting Diverse Oncogenic Factors in Tumor Cells
- Review, NA, NA
ERK↓, ERK1/2
PI3K/Akt↓,
Wnt/(β-catenin)↓,
STAT3↓,
NF-kB↓,
ChemoSen↑, cisplatin or paclitaxel, in the presence of garcinol can lead to a significant increase in the treatment outcome
COX2↓,
Casp3↑,
Casp9↑,
BAX↑,
Bcl-2↓,
VEGF↓,
TGF-β↓,
HATs↓,
E-cadherin↑,
Vim↓,
Zeb1↓,
ZEB2↓,
Let-7↑,
MMP9↓,
TumCCA↑, cycle arrest at G0/G1 phase
ROS↑,
MMP↓,
IL6↓,
NOTCH1↓,

817- GAR,    Garcinol inhibits esophageal cancer metastasis by suppressing the p300 and TGF-β1 signaling pathways
- vitro+vivo, SCC, KYSE150 - vitro+vivo, SCC, KYSE450
HATs↓, Garcinol, a natural compound extracted from Gambogic genera, is a histone acetyltransferase (HAT) inhibitor
TumCCA↑,
Apoptosis↑,
TumCMig↓,
TumCI↓,
CBP↓,
p300↓,
TGF-β↓, suppressed TGF-β1-activated Smad and non-Smad pathway
Ki-67↓,
SMAD2↓,
SMAD3↓,

796- GAR,    Polyisoprenylated benzophenone, garcinol, a natural histone acetyltransferase inhibitor, represses chromatin transcription and alters global gene expression
- vitro+vivo, Pca, HeLa
HATs↓, potent inhibitor of histone acetyltransferases p300 (IC50 approximately 7 microm)
PCAF↓,
Apoptosis↑,

832- GAR,  Rad,    Garcinol, a Histone Acetyltransferase Inhibitor, Radiosensitizes Cancer Cells by Inhibiting Non-Homologous End Joining
- in-vitro, Lung, A549 - in-vitro, NA, HeLa
HATs↓, garcinol, a HAT inhibitor
other↑, Garcinol radiosensitized A549 lung and HeLa cervical carcinoma cells with dose enhancement ratios (at 10% surviving fraction) of 1.6 and 1.5, respectively

795- GAR,    Garcinol—A Natural Histone Acetyltransferase Inhibitor and New Anti-Cancer Epigenetic Drug
- Review, NA, NA
HATs↓, HAT inhibitor
BAX↑,
PARP↑, PARP (proapoptotic) expression
Bcl-2↓,
Casp3↑,
Casp9↑,
DR5↑,
cFLIP↓,
MMP2↓,
MMP9↓,
STAT3↓,
p‑Akt↓,

2927- LT,    Luteolin Causes 5′CpG Demethylation of the Promoters of TSGs and Modulates the Aberrant Histone Modifications, Restoring the Expression of TSGs in Human Cancer Cells
- in-vitro, Cerv, HeLa
TumCMig↓, luteolin inhibited migration and colony formation in HeLa cells.
DNMTs↓, Luteolin decreased DNMT activity in HeLa cells in a concentration-dependent manner.
HDAC↓, Luteolin Decreases HDAC Activity in HeLa Cells
HATs↓, Luteolin Reduces the HAT Activity in a Dose-Dependent Manner
ac‑H3↓, H3 acetylation marks were diminished after treatment with the 20 µM of luteolin
ac‑H4↓, the acetylation marks at H4 were also modulated,
MMP2↓, Luteolin resulted in downregulation of expression of various proteins related to migration and inflammation in HeLa cells, and fold changes (FC) after treatment with 10 and 20 µM for 48 h are given, respectively, for MMP2 (FC 0.33, 0.26), MMP3 (FC 0.
MMP9↓,
HO-1↓, Genes related to cell proliferation, growth, and apoptosis such as BCL-X (FC 0.55, 0.45), HO-1/HMOX1 (FC 0.40, 0.25), Kallikrein6 (FC 0.55, 0.48), Kallikrein 3/PSA (FC 0.58, 0.48) were reduced.
E-cadherin↑, E-cadherin (FC 1.8, 2.9) were upregulated
EZH2↓, Luteolin has depicted increased expression of MiR-26a, which is a regulator of EZH2, and at the same time, it has inhibited EZH2
HER2/EBBR2↓, luteolin treatment decreased the inflammatory and migratory proteins such as MMp-2, MMP-3, HO-1/HMOX1, Her1, HER2, Her4, mesothelin, cathepsin B, MUC1, nectin 4, FOXC2, IL-18 BPa, CCL3/MIP-1α, CXCL8/IL-8, IL-2
IL18↓,
IL8↓,
IL2↓,

2448- SFN,    Sulforaphane and bladder cancer: a potential novel antitumor compound
- Review, Bladder, NA
Apoptosis↑, Recent studies have demonstrated that Sulforaphane not only induces apoptosis and cell cycle arrest in BC cells, but also inhibits the growth, invasion, and metastasis of BC cells
TumCG↓,
TumCI↓,
TumMeta↓,
glucoNG↓, Additionally, it can inhibit BC gluconeogenesis
ChemoSen↑, demonstrate definite effects when combined with chemotherapeutic drugs/carcinogens.
TumCCA↑, SFN can block the cell cycle in G2/M phase, upregulate the expression of Caspase3/7 and PARP cleavage, and downregulate the expression of Survivin, EGFR and HER2/neu
Casp3↑,
Casp7↑,
cl‑PARP↑,
survivin↓,
EGFR↓,
HER2/EBBR2↓,
ATP↓, SFN inhibits the production of ATP by inhibiting glycolysis and mitochondrial oxidative phosphorylation in BC cells in a dose-dependent manner
Glycolysis↓,
mt-OXPHOS↓,
AKT1↓, dysregulation of glucose metabolism by inhibiting the AKT1-HK2 axis
HK2↓,
Hif1a↓, Sulforaphane inhibits glycolysis by down-regulating hypoxia-induced HIF-1α
ROS↑, SFN can upregulate ROS production and Nrf2 activity
NRF2↑,
EMT↓, inhibiting EMT process through Cox-2/MMP-2, 9/ ZEB1 and Snail and miR-200c/ZEB1 pathways
COX2↓,
MMP2↓,
MMP9↓,
Zeb1↓,
Snail↓,
HDAC↓, FN modulates the histone status in BC cells by regulating specific HDAC and HATs,
HATs↓,
MMP↓, SFN upregulates ROS production, induces mitochondrial oxidative damage, mitochondrial membrane potential depolarization, cytochrome c release
Cyt‑c↓,
Shh↓, SFN significantly lowers the expression of key components of the SHH pathway (Shh, Smo, and Gli1) and inhibits tumor sphere formation, thereby suppressing the stemness of cancer cells
Smo↓,
Gli1↓,
BioAv↝, SFN is unstable in aqueous solutions and at high temperatures, sensitive to oxygen, heat and alkaline conditions, with a decrease in quantity of 20% after cooking, 36% after frying, and 88% after boiling
BioAv↝, It has been reported that the ability of individuals to use gut myrosinase to convert glucoraphanin into SFN varies widely
Dose↝, Excitingly, it has been reported that daily oral administration of 200 μM SFN in melanoma patients can achieve plasma levels of 655 ng/mL with good tolerance

5794- Sper,    Spermidine induces autophagy by inhibiting the acetyltransferase EP300
- in-vitro, Nor, U2OS
*EP300↓, potent autophagy inducers including spermidine de facto act as EP300 inhibitors.
*mTORC1↓, simultaneously inhibit mTORC1.
*CRM↑, caloric restriction or intermediate fasting,7 continuous or intermittent medication of rapamycin,8, 9, 10 administration of the sirtuin 1-activator resveratrol,11, 12 external supply of the polyamine spermidine,
*HATs↓, Spermidine turned out to be an efficient inhibitor of histone acetyltransferases in vitro
*p62↓, Moreover, all the mentioned acetyltransferase inhibitors induced a significant reduction of p62/SQSTM1 levels,
*AntiAge↑, Spermidine retards the manifestation of several major age-associated diseases including arterial aging,36 colon cancer37 and neurodegenerative processes in mice
AntiCan↑,


Showing Research Papers: 1 to 14 of 14

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 14

Pathway results for Effect on Cancer / Diseased Cells:


Redox & Oxidative Stress ⓘ

HO-1↓, 1,   NRF2↑, 1,   mt-OXPHOS↓, 1,   ROS↑, 3,  

Mitochondria & Bioenergetics ⓘ

ATP↓, 1,   MMP↓, 2,   XIAP↓, 1,  

Core Metabolism/Glycolysis ⓘ

AKT1↓, 1,   glucoNG↓, 1,   Glycolysis↓, 1,   HK2↓, 1,   PI3K/Akt↓, 1,   cl‑PPARα↓, 1,  

Cell Death ⓘ

p‑Akt↓, 1,   Apoptosis↑, 5,   BAX↑, 2,   BAX⇅, 1,   Bax:Bcl2↑, 1,   Bcl-2↓, 2,   Casp3↑, 4,   cl‑Casp3↑, 1,   Casp7↑, 1,   Casp8↑, 1,   Casp9↑, 3,   cl‑Casp9↑, 1,   CBP↓, 1,   cFLIP↓, 1,   Cyt‑c↓, 1,   Cyt‑c↑, 2,   Diablo↑, 1,   DR5↑, 1,   JNK↓, 1,   Mcl-1↓, 1,   MDM2↑, 1,   p27↑, 1,   survivin↓, 2,   Telomerase↓, 1,  

Kinase & Signal Transduction ⓘ

HER2/EBBR2↓, 2,  

Transcription & Epigenetics ⓘ

EZH2↓, 1,   ac‑H3↓, 1,   ac‑H3↑, 1,   ac‑H4↓, 1,   ac‑H4↑, 1,   HATs↓, 11,   other↑, 1,   PCAF↓, 1,   pRB↑, 1,  

DNA Damage & Repair ⓘ

DNMT1↓, 1,   DNMTs↓, 3,   p16↑, 1,   P53↑, 1,   PARP↑, 1,   cl‑PARP↑, 1,   PCNA↓, 1,  

Cell Cycle & Senescence ⓘ

CDK2↓, 1,   CDK4↓, 1,   cycD1/CCND1↓, 1,   cycE/CCNE↓, 1,   P21↑, 1,   TumCCA↑, 4,  

Proliferation, Differentiation & Cell State ⓘ

cFos↓, 1,   CREB2↓, 1,   EMT↓, 1,   ERK↓, 1,   FOXO↑, 1,   Gli1↓, 1,   HDAC↓, 4,   HDAC1↓, 1,   HDAC3↓, 1,   HDAC8↓, 1,   Let-7↑, 1,   NOTCH1↓, 1,   p300↓, 2,   Shh↓, 1,   Smo↓, 1,   STAT3↓, 2,   TumCG↓, 1,   Wnt/(β-catenin)↓, 1,  

Migration ⓘ

AP-1↓, 1,   E-cadherin↑, 2,   FAK↓, 1,   Ki-67↓, 1,   MMP2↓, 4,   MMP9↓, 5,   MMPs↓, 1,   PDGF↓, 1,   RECK↑, 1,   SMAD2↓, 1,   SMAD3↓, 1,   Snail↓, 1,   TGF-β↓, 2,   TIMP2↑, 1,   TumCI↓, 3,   TumCMig↓, 2,   TumCP↓, 2,   TumMeta↓, 2,   uPA↓, 1,   Vim↓, 1,   Zeb1↓, 2,   ZEB2↓, 1,  

Angiogenesis & Vasculature ⓘ

angioG↓, 2,   EGFR↓, 2,   Hif1a↓, 2,   VEGF↓, 2,  

Immune & Inflammatory Signaling ⓘ

COX2↓, 5,   IL18↓, 1,   IL2↓, 1,   IL6↓, 2,   IL8↓, 1,   IκB↑, 1,   NF-kB↓, 5,   TNF-α↓, 1,  

Hormonal & Nuclear Receptors ⓘ

CDK6↓, 1,  

Drug Metabolism & Resistance ⓘ

BioAv↝, 2,   ChemoSen↑, 2,   Dose↑, 1,   Dose↝, 1,   eff↑, 1,   selectivity↑, 2,  

Clinical Biomarkers ⓘ

EGFR↓, 2,   EZH2↓, 1,   HER2/EBBR2↓, 2,   IL6↓, 2,   Ki-67↓, 1,   NOS2↓, 1,  

Functional Outcomes ⓘ

AntiCan↑, 1,  
Total Targets: 126

Pathway results for Effect on Normal Cells:


Redox & Oxidative Stress ⓘ

antiOx↑, 2,   ROS↓, 2,  

Core Metabolism/Glycolysis ⓘ

CRM↑, 2,  

Transcription & Epigenetics ⓘ

HATs↓, 3,  

Autophagy & Lysosomes ⓘ

p62↓, 1,  

Proliferation, Differentiation & Cell State ⓘ

EP300↓, 2,   HDAC↑, 1,   mTORC1↓, 1,  

Migration ⓘ

AP-1↓, 1,  

Angiogenesis & Vasculature ⓘ

angioG↓, 1,  

Immune & Inflammatory Signaling ⓘ

Inflam↓, 1,   NF-kB↓, 2,  

Protein Aggregation ⓘ

Aβ↓, 1,  

Drug Metabolism & Resistance ⓘ

BioAv↓, 1,  

Functional Outcomes ⓘ

AntiAge↑, 1,   cognitive↑, 1,   neuroP↑, 1,   toxicity↓, 1,  
Total Targets: 18

Scientific Paper Hit Count for: HATs, histone acetyltransferases
5 Garcinol
2 Curcumin
2 EGCG (Epigallocatechin Gallate)
1 Andrographis
1 Aspirin -acetylsalicylic acid
1 Cisplatin
1 Paclitaxel
1 Radiotherapy/Radiation
1 Luteolin
1 Sulforaphane (mainly Broccoli)
1 Spermidine
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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