ACLY Cancer Research Results

ACLY, ATP citrate lyase: Click to Expand ⟱
Source:
Type:
ACLY links energy metabolism provided by catabolic pathways to biosynthesis. ACLY, which has been found to be overexpressed in many cancers, converts citrate into acetyl-CoA and OAA.ATP citrate lyase exhibited upregulation in various tumours.
General Tumour Biomarker
•ACLY is a key enzyme in cancer metabolism.
•ACLY is involved in glucose and lipid metabolism.
•Many ACLY inhibitors were developed as anti-cancer agents.

ACLY is a key enzyme in cellular metabolism that converts citrate into acetyl‐CoA and oxaloacetate. Acetyl‐CoA is a substrate for lipid synthesis and protein acetylation, processes that are often upregulated in cancer cells to support rapid growth and proliferation.

ACLY is found overexpressed in many aggressive cancers. ACLY abundantly consumes citrate from nutrient catabolism (especially glucose and glutamine) to support protein acetylation and intense nucleotide and lipid synthesis. The significant decrease in cytosolic citrate appears to play a central role in cancer metabolism by enhancing the Warburg effect and activating the PI3K / AKT axis promoting ACLY activity in a feedback loop. Thus, the inhibition of factors regulating its expression (such as SREBP1) and its activation (such as AKT) could have an anti-proliferative effect.

Elevated ACLY expression has been observed in a number of cancers. In many studies, high levels of ACLY have been associated with more aggressive disease and poorer prognoses.

Natural ACLY Inhibitors
-Hydroxycitrate (HCA):(widely studied)
-EGCG
-Quercetin
-Resveratrol
-Luteolin
-Citrate
-Cucurbitacin B
-Emodin?
Scientific Papers found: Click to Expand⟱
7503- H2S,    Hydrogen Sulfide, an Endogenous Stimulator of Mitochondrial Function in Cancer Cells
- Review, Var, NA
DNArepair↑, endogenous H2S in cancer cells include the maintenance of mitochondrial organization (protection against mitochondrial fission) and the maintenance of mitochondrial DNA repair
CBS↑, CBS is upregulated and H2S generation is increased in primary human colon cancer tissues compared to the surrounding (nominally healthy) tissues
3MST/MPST↑, it is now clear that CBS, and/or CSE and/or 3-MST is overexpressed in many forms of cancer.
ETC↑, H2S can enhance mitochondrial electron transport and ATP production in cancer cells are shown in Figure 1.
ATP↑,
Glycolysis↑, H2S can also stimulate glycolysis (another key energetic process in cancer cells
ACLY↑, recently discovered mechanism relates to the upregulation of ACLY by H2S


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) ⓘ

3MST/MPST↑, 1,   CBS↑, 1,  

Mitochondria & Bioenergetics(tgid=3) ⓘ

ATP↑, 1,   ETC↑, 1,  

Core Metabolism/Glycolysis(tgid=4) ⓘ

ACLY↑, 1,   Glycolysis↑, 1,  

DNA Damage & Repair(tgid=10) ⓘ

DNArepair↑, 1,  
Total Targets: 7

Pathway results for Effect on Normal Cells:


Total Targets: 0

Scientific Paper Hit Count for: ACLY, ATP citrate lyase
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#:2  State#:%  Dir#:2
  wNotes=on  sortOrder:rid,rpid

 

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