NAT Cancer Research Results

NAT, N-acetyltransferase: Click to Expand ⟱
Source:
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N-acetyltransferase (NAT) refers to enzymes that transfer an acetyl group from acetyl-CoA to nitrogen-containing substrates. In xenobiotic metabolism, the principal human arylamine N-acetyltransferases are NAT1 and NAT2. They metabolize drugs, aromatic amines, and heterocyclic amines through N-acetylation and O-acetylation, thereby contributing to either detoxification or metabolic activation of carcinogens. NAT activity and genetic polymorphisms can therefore influence drug response and cancer susceptibility. The direction is context-dependent: increased NAT activity may enhance detoxification of some compounds but activate other procarcinogens. NAT1, NAT2, or total NAT activity is study specific, and protein N-terminal acetyltransferases such as NAA10 are separate targets. NAT1 reference; NAT2 reference; Cancer review.



Scientific Papers found: Click to Expand⟱
6833- EMD,    Anticancer potential of emodin
- Review, Var, NA
Inflam↓, emodin demonstrates anti-neoplastic, anti-inflammatory, anti-angiogenesis, and toxicological potential for use in pharmacology, both in vitro and in vivo
angioG↓,
TumCCA↑, Emodin demonstrates cytotoxic effects (e.g., cell death) through the arrest of the cell cycle and the induction of apoptosis in cancer cells.
Apoptosis↑,
HIF-1↓, As a novel inhibitor of HIF-1, emodin is an adjunct that boosts the efficacy of cytotoxic drugs used for the treatment of prostate cancer DU-145 cells,
TumCI↓, while inhibiting angiogenesis, invasion, migration, chemical-induced carcinogen-DNA adduct formation, HER2/neu, CKII kinase, and p34cdc2 kinase in human cancer cells.
TumCMig↓,
HER2/EBBR2↓,
CK2↓,
ROS↑, In addition, emodin enhances arsenic trioxide-induced apoptosis by generating ROS and inhibiting survival signaling
AR↓, Emodin downregulates androgen receptors and inhibits the cellular growth of prostate cancer
JAK2↓, Emodin selectively inhibits the interleukin–6-induced JAK2/STAT3 pathway and induces apoptosis in myeloma cells via the downregulation of myeloid cell leukemia 1 (Mcl-1) cells
STAT3↓,
Mcl-1↓,
NAT↓, emodin and aloe-emodin inhibit N-acetyltransferase (NAT) activity and gene expression in mouse leukemia L1210 cells
ChemoSen↑, Emodin enhances apoptosis in cisplatin-induced gallbladder carcinomas in a ROS-dependent manner and suppresses survivin expression
survivin↓,
XIAP↓, Emodin downregulates X-linked inhibitor of apoptosis protein (XIAP) expression [84] and inhibits NF-κB against human pancreatic cancer
NF-kB↓,
*neuroP↑, Emodin induces apoptosis in the mouse microglial BV-2 cell line via Tribbles homolog 3 (TRB3) and eliminates inflammatory microglia, thereby exerting neuroprotective effects
*hepatoP↑, Emodin also demonstrates hepatoprotective effects against CCl4-induced liver injury


Showing Research Papers: 1 to 1 of 1

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 1

Pathway results for Effect on Cancer / Diseased Cells:


NA, unassigned(tgid=0) ⓘ

NAT↓, 1,  

Redox & Oxidative Stress(tgid=1) ⓘ

ROS↑, 1,  

Mitochondria & Bioenergetics(tgid=3) ⓘ

XIAP↓, 1,  

Cell Death(tgid=5) ⓘ

Apoptosis↑, 1,   CK2↓, 1,   Mcl-1↓, 1,   survivin↓, 1,  

Kinase & Signal Transduction(tgid=6) ⓘ

HER2/EBBR2↓, 1,  

Cell Cycle & Senescence(tgid=11) ⓘ

TumCCA↑, 1,  

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

STAT3↓, 1,  

Migration(tgid=13) ⓘ

TumCI↓, 1,   TumCMig↓, 1,  

Angiogenesis & Vasculature(tgid=14) ⓘ

angioG↓, 1,   HIF-1↓, 1,  

Immune & Inflammatory Signaling(tgid=16) ⓘ

Inflam↓, 1,   JAK2↓, 1,   NF-kB↓, 1,  

Hormonal & Nuclear Receptors(tgid=20) ⓘ

AR↓, 1,  

Drug Metabolism & Resistance(tgid=21) ⓘ

ChemoSen↑, 1,  

Clinical Biomarkers(tgid=22) ⓘ

AR↓, 1,   HER2/EBBR2↓, 1,  
Total Targets: 21

Pathway results for Effect on Normal Cells:


Functional Outcomes(tgid=23) ⓘ

hepatoP↑, 1,   neuroP↑, 1,  
Total Targets: 2

Scientific Paper Hit Count for: NAT, N-acetyltransferase
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#:1532  State#:%  Dir#:1
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