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⟱
3437- ALA,    Revisiting the molecular mechanisms of Alpha Lipoic Acid (ALA) actions on metabolism
- Review, Var, NA
*IronCh↑, ALA functions as a metabolic regulator, metal chelator, and a powerful antioxidant.
*antiOx↑,
*ROS↓, It quenches reactive oxygen species (ROS), restores exogenous and endogenous antioxidants such as vitamins and Glutathione (GSH), and repairs oxidized proteins
*GSH↑,
*NF-kB↓, inhibition of the activation of nuclear factor kappa B (NF-κB)
*AMPK⇅, activation of peripheral AMPK and inhibition of hypothalamic AMPK
*FAO↑, ALA has been found to activate peripheral AMPK, thereby enhancing fatty acid oxidation and glucose uptake in muscle cells
*GlucoseCon↑,
*PI3K↑, It stimulates glucose uptake by increasing the activity of PI3K and Akt which are crucial for the translocation of glucose transporters like GLUT4 to the cell membrane, mimicking the action of insulin
*Akt?,

5381- ART/DHA,    Artemisitene triggers calcium-dependent ferroptosis by disrupting the LSH-EWSR1 interaction in colorectal cancer
- in-vitro, CRC, HCT116 - in-vitro, Nor, NCM460 - in-vitro, CRC, HT29 - in-vitro, CRC, HCT8
Ferroptosis↑, Artemisia annua, acted as a CRC therapeutic agent by promoting calcium-dependent ferroptosis.
CYP24A1↓, ATT repressed cytochrome P450 family 24 subfamily A member 1 (CYP24A1) expression, the pivotal mediator of this response
Ca+2↑, ATT downregulated CYP24A1 expression to elevate calcium levels and induce ferroptosis in CRC cells
SCD1↓, The ensuing calcium overload downregulated stearoyl-CoA desaturase (SCD) by CAMKK2/AMPK/SREBF1 axis, enriching oxidizable fatty acids and sensitizing CRC cells to lethal lipid peroxidation.
FAO↑,
lipid-P↑,
eff↑, The results showed that ATT exhibited the highest cytotoxicity, surpassing that of dihydroartemisinin and artesunate, whereas artemisinin and artemether were only weakly effective
selectivity↑, ATT induced cell death in a strictly time-dependent manner and displayed minimal toxicity toward normal NCM460 epithelial cells
other?, Collectively, these data reveal that ATT-driven calcium overload disrupts fatty-acid homeostasis via SCD inhibition, thereby steering CRC cells toward ferroptosis.

2389- BA,    Baicalin alleviates lipid accumulation in adipocytes via inducing metabolic reprogramming and targeting Adenosine A1 receptor
- in-vitro, Obesity, 3T3
*ECAR↑, Baicalin promoted metabolic reprogramming in 3T3-L1 preadipocytes, characterized by increased ECAR and decreased OCR
*OCR↓,
*p‑AMPK↑, baicalin significantly altered cellular respiration by reducing mitochondrial oxygen consumption while enhancing glycolytic flux, accompanied by increased phosphorylation of AMPK and ACC, suggesting an adaptation to altered energy availability.
*p‑ACC↑,
*Glycolysis↑, significant enrichment in metabolic pathways such as glycolysis, gluconeogenesis, and lipid metabolism.
*lipidDe↓, inhibited the maturation of sterol regulatory element binding protein 1 (SREBP1) and finally alleviated lipid deposition.
*SREBP1↓,
*FAO↑, baicalin induces metabolic reprogramming of adipocytes by inhibiting glucose aerobic metabolism while enhancing anaerobic glycolysis and FAO.
*HK2↑, baicalin upregulated glycolytic enzymes, such as HK1, HK2, PKM2, and LDHA, while downregulating pyruvate dehydrogenase,
*PKM2↑,
*LDHA↑,
*PDKs↓,
*ACC↓, leading to decreased acetyl-CoA production and enhanced fatty acid β-oxidation.

2348- CAP,    Recent advances in analysis of capsaicin and its effects on metabolic pathways by mass spectrometry
- Analysis, Nor, NA
Warburg↓, Capsaicin inhibits the Warburg effect by binding directly to Cys424 residue and LDHA of pyruvate kinase isoenzyme type M2 (PKM2).
*PKM2↓,
*COX2↓, capsaicin targets COX-2 and down-regulates its expression, which results in the further inhibition of inflammation
*Inflam↓,
*Sepsis↓, capsaicin may be used as a new active ingredient to treat sepsis and inflammation
*AMPK↑, capsaicin activates adenylate-activated protein kinase (AMPK) and protein kinase A (PKA), in turn enhancing the activity of the mitochondrial respiratory chain and promoting fatty acid oxidation
*PKA↑,
*mitResp↑,
*FAO↑,
*FASN↓, capsaicin can inhibit the activity of fatty acid synthetase
*PGM1?,
*ATP↑, treatment resulted in increased intracellular ATP levels (the end product of glycolysis)
*ROS↓, Capsaicin can mitigate the negative effects of oxidative stress on human health by scavenging these free radicals and reducing the oxidative stress response.

2247- MF,    Effects of Pulsed Electromagnetic Field Treatment on Skeletal Muscle Tissue Recovery in a Rat Model of Collagenase-Induced Tendinopathy: Results from a Proteome Analysis
- in-vivo, Nor, NA
*Glycolysis↓, PEMF-treated animals exhibited decreased glycolysis and increased LDHB expression, enhancing NAD signaling and ATP production
*LDHB↑,
*NAD↑,
*ATP↑,
*antiOx↑, Antioxidant protein levels increased, controlling ROS production.
*ROS↑,
*YAP/TEAD↑, upregulation of YAP and PGC1alpha and increasing slow myosin isoforms, thus speeding up physiological recovery.
*PGC-1α↑,
*TCA↑, increased in PEMF-treated injured limbs
*FAO↑,
*OXPHOS↑, Oxidative phosphorylation was increased in the muscle of injured rats that underwent PEMF treatment

2052- PB,    Lipid-regulating properties of butyric acid and 4-phenylbutyric acid: Molecular mechanisms and therapeutic applications
- Review, NA, NA
*HDAC↓, BA appears to function as a histone deacetylase (HDAC) inhibitor while PBA acts as a chemical chaperone and/or a HDAC inhibitor.
*Half-Life↑, In humans, the plasma concentration of BA decreased quickly with a half-life of approximately 5 min once the infusion had ended
*Half-Life↑, The mean half-lives of PBA, PAA and PAGN in blood plasma were 0.7, 1.2 and 1.7 h, respectively, after an intravenous infusion of sodium phenylbutyrate to human subjects and 1, 1.8 and 2.8 h in serum, respectively, after an oral PB 9 to 45 g/day
*lipoGen↓, in vivo studies have shown that PBA ameliorated fructose-induced hepatosteatosis by inhibiting lipogenesis.
*ER Stress↓, PBA blocked fructose-driven expression of SREBP1c and its target genes by attenuating ER stres
*FAO↑, BA and PBA promote fatty acid β-oxidation
*ROS↓, Moreover, PBA prevented palmitate-induced autophagy-dependent reactive oxygen species (ROS) formation further supporting the protective role of PBA against lipotoxicity.
*BioAv↑, The absolute bioavailability of PBA averaged 78% in human subjects following the oral administrations of 9-45 g/day

4284- RES,    Resveratrol induces dephosphorylation of Tau by interfering with the MID1-PP2A complex
- in-vitro, AD, HEK293 - NA, Stroke, NA - in-vivo, AD, NA
*p‑tau↓, Resveratrol induces dephosphorylation of Tau
*PP2A↑, resveratrol, a polyphenol, significantly induces PP2A activity and reduces Tau phosphorylation at PP2A-dependent epitopes.
*neuroP↑, resveratrol is more and more being established as a neuroprotective drug after ischemic brain injury and in neurodegenerative disorders including Parkinson’s Disease13,14, AD15,16 and Huntington’s Disease
*antiOx↑, resveratrol has anti-oxidant activity19,20, inhibits cycloxygenase activity21,22, ribonucleotide reductase23, protein kinase C24, DNA polymerase 25 and has antiestrogenic properties26,27 and anti-platelet activity
COX2↓,
*AntiAg↑,
*SIRT1↑, it activates Sirt1, an NAD+-dependent protein deacetylase28,29 and also has been demonstrated to activate AMP kinase (AMPK)30,31, an important glucose sensor that inhibits acetyl-CoA carboxylase, thereby increasing oxidation of fatty acids and decre
*AMPK↑,
*Acetyl-CoA↓,
*FAO↑,
*ADAM10↑, Resveratrol has been suggested to induce the α-secretase ADAM10, which outcompetes BACE1 and thereby reduces Aβ-production
*BACE↓,
*Aβ↓,
*memory↑, interestingly, the resveratrol-mediated reduction of Aβ increases life span and improves learning and memory
*Inflam↓, reduces neuroinflammation47 and reduces oxidative stress48.
*ROS↓,

4893- Sper,  immuno,    Chemoproteomic Identification of Spermidine-Binding Proteins and Antitumor-Immunity Activators
- in-vitro, Var, NA
*mt-FAO↑, Spermidine, a biogenic polyamine that declines along with aging, shows promise in restoring antitumor immunity by enhancing mitochondrial fatty acid oxidation (FAO)
eff↑, This study lays the foundation for developing small-molecule activators of antitumor immunity, offering potential in combination cancer immunotherapy.

2411- UA,    Ursolic acid in health and disease
- Review, Var, NA
Inflam↓, UA because of its beneficial effects, which include anti-inflammatory, anti-oxidant, anti-apoptotic, and anti-carcinogenic effects
antiOx↑,
NF-kB↓, Colon cancer HCT116, HT29 20 μM for 8 hour ↓ NF-kB, Bcl-xL, Bcl-2, and cyclin D1
Bcl-xL↓,
Bcl-2↓,
cycD1/CCND1↓,
Ki-67↓, ↓ Ki67, CD31, STAT3, and EGFR, ↑ p53 and p21 mRNA expression
CD31↓,
STAT3↓,
EGFR↓,
P53↑,
P21↓,
HK2↓, MCF-7, MDA-MB-231 20 μM for 24 hours ↓ HK2, PKM2, ATP, and lactate ↓ pERK1/2, and depolarization of mitochondrial membrane potential, ↑ Nitric oxide and ATM
PKM2↓,
ATP↓,
lactateProd↓,
p‑ERK↓,
MMP↓,
NO↑,
ATM↑,
Casp3↑, T24 cancer cells ↑ Caspase 3 activity ↑ AMPK activation ↑ JNK activation
AMPK↑,
JNK↑,
FAO↑, 80 μM UA reduces triglyceride (TG) and cholesterol levels by increasing fatty acid oxidation and decreasing fatty acid synthesis in hepatocytes
FASN↓,
*GSH↑, ↑ Vitamin C, E, GSH, SOD, CAT, GPx, GST, and GR in heart
*SOD↑,
*Catalase↑,
*GPx↑,
*GSTs↑,
neuroP↑, This demonstrates that UA has a protective effect against various inflammatory conditions of the brain.


Showing Research Papers: 1 to 9 of 9

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 9

Pathway results for Effect on Cancer / Diseased Cells:


Redox & Oxidative Stress ⓘ

antiOx↑, 1,   Ferroptosis↑, 1,   lipid-P↑, 1,  

Mitochondria & Bioenergetics ⓘ

ATP↓, 1,   MMP↓, 1,  

Core Metabolism/Glycolysis ⓘ

AMPK↑, 1,   FAO↑, 2,   FASN↓, 1,   HK2↓, 1,   lactateProd↓, 1,   PKM2↓, 1,   SCD1↓, 1,   Warburg↓, 1,  

Cell Death ⓘ

Bcl-2↓, 1,   Bcl-xL↓, 1,   Casp3↑, 1,   Ferroptosis↑, 1,   JNK↑, 1,  

Transcription & Epigenetics ⓘ

other?, 1,  

DNA Damage & Repair ⓘ

ATM↑, 1,   P53↑, 1,  

Cell Cycle & Senescence ⓘ

cycD1/CCND1↓, 1,   P21↓, 1,  

Proliferation, Differentiation & Cell State ⓘ

p‑ERK↓, 1,   STAT3↓, 1,  

Migration ⓘ

Ca+2↑, 1,   CD31↓, 1,   Ki-67↓, 1,  

Angiogenesis & Vasculature ⓘ

EGFR↓, 1,   NO↑, 1,  

Immune & Inflammatory Signaling ⓘ

COX2↓, 1,   Inflam↓, 1,   NF-kB↓, 1,  

Hormonal & Nuclear Receptors ⓘ

CYP24A1↓, 1,  

Drug Metabolism & Resistance ⓘ

eff↑, 2,   selectivity↑, 1,  

Clinical Biomarkers ⓘ

EGFR↓, 1,   Ki-67↓, 1,  

Functional Outcomes ⓘ

neuroP↑, 1,  
Total Targets: 39

Pathway results for Effect on Normal Cells:


Redox & Oxidative Stress ⓘ

antiOx↑, 3,   Catalase↑, 1,   GPx↑, 1,   GSH↑, 2,   GSTs↑, 1,   lipidDe↓, 1,   OXPHOS↑, 1,   ROS↓, 4,   ROS↑, 1,   SOD↑, 1,  

Metal & Cofactor Biology ⓘ

IronCh↑, 1,  

Mitochondria & Bioenergetics ⓘ

ATP↑, 2,   mitResp↑, 1,   OCR↓, 1,   PGC-1α↑, 1,  

Core Metabolism/Glycolysis ⓘ

ACC↓, 1,   p‑ACC↑, 1,   Acetyl-CoA↓, 1,   AMPK↑, 2,   AMPK⇅, 1,   p‑AMPK↑, 1,   ECAR↑, 1,   FAO↑, 6,   mt-FAO↑, 1,   FASN↓, 1,   GlucoseCon↑, 1,   Glycolysis↓, 1,   Glycolysis↑, 1,   HK2↑, 1,   LDHA↑, 1,   LDHB↑, 1,   lipoGen↓, 1,   NAD↑, 1,   PDKs↓, 1,   PGM1?, 1,   PKM2↓, 1,   PKM2↑, 1,   SIRT1↑, 1,   SREBP1↓, 1,   TCA↑, 1,  

Cell Death ⓘ

Akt?, 1,   YAP/TEAD↑, 1,  

Protein Folding & ER Stress ⓘ

ER Stress↓, 1,  

Proliferation, Differentiation & Cell State ⓘ

HDAC↓, 1,   PI3K↑, 1,  

Migration ⓘ

AntiAg↑, 1,   PKA↑, 1,  

Immune & Inflammatory Signaling ⓘ

COX2↓, 1,   Inflam↓, 2,   NF-kB↓, 1,  

Synaptic & Neurotransmission ⓘ

ADAM10↑, 1,   p‑tau↓, 1,  

Protein Aggregation ⓘ

Aβ↓, 1,   BACE↓, 1,   PP2A↑, 1,  

Drug Metabolism & Resistance ⓘ

BioAv↑, 1,   Half-Life↑, 2,  

Functional Outcomes ⓘ

memory↑, 1,   neuroP↑, 1,  

Infection & Microbiome ⓘ

Sepsis↓, 1,  
Total Targets: 60

Scientific Paper Hit Count for: FAO, Fatty Acid Oxidation
1 Alpha-Lipoic-Acid
1 Artemisinin
1 Baicalin
1 Capsaicin
1 Magnetic Fields
1 Phenylbutyrate
1 Resveratrol
1 Spermidine
1 immunotherapy
1 Ursolic acid
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#:2
  wNotes=on  sortOrder:rid,rpid

 

Home Page