FAO Cancer Research Results

FAO, Fatty Acid Oxidation: Click to Expand ⟱
Source:
Type:
FAO (also known as β-oxidation) is a metabolic process in which fatty acids are broken down in the mitochondria (and, to a lesser extent, in peroxisomes) to generate acetyl-CoA. This acetyl-CoA then enters the tricarboxylic acid (TCA) cycle, ultimately driving the production of ATP via oxidative phosphorylation. FAO is crucial for energy production, especially under conditions where carbohydrates are scarce.

While many cancer cells are known for their reliance on glycolysis (the Warburg effect), some tumors exploit FAO to meet their energy needs. FAO can provide a high yield of ATP, which is particularly valuable in nutrient-deprived or hypoxic microenvironments. Tumor cells with high FAO activity may use it to sustain survival, promote proliferation, and support metastatic processes.

High FAO activity has been correlated with aggressive tumor behavior and poorer prognosis in certain cancers. Enhanced FAO may support survival under metabolic stress and contribute to resistance against treatments that target glycolytic pathways. Thus, tumors with elevated FAO could potentially be more difficult to treat.


Scientific Papers found: Click to Expand⟱
2740- BetA,    Effects and mechanisms of fatty acid metabolism-mediated glycolysis regulated by betulinic acid-loaded nanoliposomes in colorectal cancer
- in-vitro, CRC, HCT116
TumCP↓, Glycolysis↓, HK2↓, PFK1↓, PKM2↓, ACSL1↓, CPT1A↓, FASN↓, FAO↓, GlucoseCon↓, lactateProd↓,
3761- H2,    Therapeutic Inhalation of Hydrogen Gas for Alzheimer's Disease Patients and Subsequent Long-Term Follow-Up as a Disease-Modifying Treatment: An Open Label Pilot Study
- Human, AD, NA
*cognitive↑, *BBB↑, *ROS↓, *NRF2↑, *Inflam↓, *NFAT↓, *FAO↓, *4-HNE↓, *PGC-1α↑, *Ferroptosis↓,
2248- MF,    Magnetic fields modulate metabolism and gut microbiome in correlation with Pgc-1α expression: Follow-up to an in vitro magnetic mitohormetic study
- in-vivo, Nor, NA
*PGC-1α↑, *GutMicro↑, *FAO↓, *Insulin↓,
1201- QC,    Quercetin: a silent retarder of fatty acid oxidation in breast cancer metastasis through steering of mitochondrial CPT1
- in-vivo, BC, NA
mitResp↓, Glycolysis↓, ATP↓, ROS↑, GSH↓, TumMeta↓, Apoptosis↑, FAO↓,

Showing Research Papers: 1 to 4 of 4

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 4

Pathway results for Effect on Cancer / Diseased Cells:


Redox & Oxidative Stress

GSH↓, 1,   ROS↑, 1,  

Mitochondria & Bioenergetics

ATP↓, 1,   mitResp↓, 1,  

Core Metabolism/Glycolysis

ACSL1↓, 1,   CPT1A↓, 1,   FAO↓, 2,   FASN↓, 1,   GlucoseCon↓, 1,   Glycolysis↓, 2,   HK2↓, 1,   lactateProd↓, 1,   PFK1↓, 1,   PKM2↓, 1,  

Cell Death

Apoptosis↑, 1,  

Migration

TumCP↓, 1,   TumMeta↓, 1,  
Total Targets: 17

Pathway results for Effect on Normal Cells:


Redox & Oxidative Stress

4-HNE↓, 1,   Ferroptosis↓, 1,   NRF2↑, 1,   ROS↓, 1,  

Mitochondria & Bioenergetics

Insulin↓, 1,   PGC-1α↑, 2,  

Core Metabolism/Glycolysis

FAO↓, 2,  

Cell Death

Ferroptosis↓, 1,  

Migration

NFAT↓, 1,  

Barriers & Transport

BBB↑, 1,  

Immune & Inflammatory Signaling

Inflam↓, 1,  

Clinical Biomarkers

GutMicro↑, 1,  

Functional Outcomes

cognitive↑, 1,  
Total Targets: 13

Scientific Paper Hit Count for: FAO, Fatty Acid Oxidation
1 Betulinic acid
1 Hydrogen Gas
1 Magnetic Fields
1 Quercetin
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#:1044  State#:%  Dir#:1
wNotes=0 sortOrder:rid,rpid

 

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