OAA Cancer Research Results

OAA, oxaloacetate: Click to Expand ⟱
Source:
Type:
OAA is not an enzyme or protein but a key metabolic intermediate. OAA plays a central role in multiple metabolic pathways, including the tricarboxylic acid (TCA) cycle and gluconeogenesis, rather than being “expressed” in the traditional sense.

-OAA is an intermediate in the TCA cycle (citric acid cycle), which is crucial for energy production in cells.
-It also serves as a substrate for gluconeogenesis (conversion into phosphoenolpyruvate by PEPCK) and amino acid biosynthesis.
-Because of its central metabolic position, changes in OAA availability can affect the balance between oxidative phosphorylation and glycolysis—a balance that is often disrupted in cancer cells (the Warburg effect).

-Upregulation of pyruvate carboxylase (which converts pyruvate to OAA) has been associated with aggressive tumor behavior in certain cancers (e.g., lung and breast cancers).
-Similarly, altered malate dehydrogenase activity, which interconverts malate and OAA, has also been linked to metabolic shifts in cancer cells that correlate with prognosis.
-These associations are often interpreted as markers of metabolic reprogramming rather than direct “OAA expression.”

-Altered activities of enzymes that govern OAA production or utilization are associated with aggressive tumor phenotypes, making them of interest both as potential prognostic biomarkers and as therapeutic targets.
Scientific Papers found: Click to Expand⟱
1586- Citrate,    Extracellular Citrate Is a Trojan Horse for Cancer Cells
- in-vitro, Liver, HepG2
Dose?, At low concentration, citrate increased both histone H4 acetylation and lipid deposition; at high concentration, citrate inhibited both
ac‑H4↓,
lipidDe↓,
ACLY↓, Considering the strong demand for acetyl-CoA but not for OAA in tumor cells, the exogenous citrate would behave like a trojan horse that carries OAA inside the cells and reduces ACLY expression and cellular metabolism.
selectivity↑, in non-tumor cells, changes of acetylated histone level do not correspond to a change of ACLY expression, as instead shown by HepG2 cells.
*ACLY∅, In contrast, ACLY expression in IHH (normal)cells was not modified after citrate exposure, suggesting that, in this case, ACLY expression was not regulated by histone H4 acetylation
Glycolysis↓, strong inhibition of glycolysis, which leads to a decrease in NADH necessary for OAA reduction
NADH↓,
OAA↑, exogenous citrate would behave like a trojan horse that releases OAA in the cells, where it could exert its therapeutic effect also on hepatoma cells.
other↑, most important discovery is undoubtedly the demonstration that high concentrations of citrate decrease the availability of acetyl-CoA, a key molecule both in the metabolism of sugars and lipids


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:


Redox & Oxidative Stress ⓘ

lipidDe↓, 1,   NADH↓, 1,  

Core Metabolism/Glycolysis ⓘ

ACLY↓, 1,   Glycolysis↓, 1,   OAA↑, 1,  

Transcription & Epigenetics ⓘ

ac‑H4↓, 1,   other↑, 1,  

Drug Metabolism & Resistance ⓘ

Dose?, 1,   selectivity↑, 1,  
Total Targets: 9

Pathway results for Effect on Normal Cells:


Core Metabolism/Glycolysis ⓘ

ACLY∅, 1,  
Total Targets: 1

Scientific Paper Hit Count for: OAA, oxaloacetate
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#:1148  State#:%  Dir#:2
  wNotes=on  sortOrder:rid,rpid

 

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