Melatonin / FAO Cancer Research Results

MEL, Melatonin: Click to Expand ⟱
Features:
Hormone in the body made by pineal gland.
• Melatonin is a potent antioxidant. It neutralizes reactive oxygen species (ROS) and reactive nitrogen species (RNS), which are involved in DNA damage and cancer progression.
• Melatonin has been shown to modulate apoptotic pathways by influencing mitochondrial permeability, cytochrome c release, and caspase activation.
• In several cancer cell models, melatonin appears to promote apoptosis in malignant cells while sparing normal cells.

The most well-known indolamines are serotonin and melatonin, both of which play significant roles in regulating mood, sleep, and overall mental well-being.

Melatonin doses (20 mg to even 40 mg per day), often given as an adjuvant treatment for cancer.
-The plasma half-life of melatonin is generally in the range of approximately 20 to 60 minutes
-It has been suggested that administering melatonin at the appropriate phase of the circadian cycle may enhance its anti-tumor activity and reduce the side effects of chemotherapy and radiation therapy.

Bio-availability: Oral melatonin has a low and variable bio-availability (often estimated between 3% and 33%), which means that only a fraction of the ingested dose reaches the bloodstream unchanged.

For proOxidant effect might need >10uM, which might be 100mg dose (assuming 10% bio-availability) Might also be required X10 levels?
-It remains unknown whether the pro-oxidant action exists in vivo. the vast majority of evidence indicates that melatonin is a potent antioxidant in vivo even at pharmacological concentrations.

Interactions:
-Melatonin could potentially add to the blood pressure–lowering properties of antihypertensive drugs.
-Patients using insulin should be monitored for changes in blood glucose levels.
-Melatonin might interact with drugs like warfarin, aspirin, or clopidogrel.(antiplatelet)


Melatonin Cancer Relevant Pathways
Rank Pathway / Axis Cancer Cells Normal Cells Label Primary Interpretation Notes
1 Circadian signaling (MT1 / MT2 receptors) ↓ proliferative circadian disruption ↑ circadian synchronization Driver Chronobiology normalization Melatonin restores circadian control; cancer cells lose growth advantages from circadian dysregulation
2 Reactive oxygen species (ROS) ↓ ROS (baseline); context-dependent ↑ stress signaling ↓ ROS (strong buffering) Driver Antioxidant dominance with signaling effects Melatonin is a potent direct and indirect antioxidant; cancer cells may still undergo stress-mediated growth inhibition
3 Mitochondrial function ↓ metabolic flexibility; ↑ apoptosis sensitivity ↑ mitochondrial efficiency Secondary Mitochondrial stabilization vs vulnerability Melatonin improves mitochondrial function in normal cells while limiting metabolic plasticity in cancer cells
4 Estrogen signaling (ERα modulation) ↓ estrogen-driven proliferation ↔ minimal Secondary Hormone-dependent growth suppression Particularly relevant in breast and hormone-responsive cancers
5 NF-κB signaling ↓ inflammatory / survival signaling ↓ inflammatory tone Secondary Anti-inflammatory modulation NF-κB suppression contributes to reduced tumor-promoting inflammation
6 Cell cycle regulation ↓ proliferation / ↑ arrest ↔ spared Phenotypic Cytostatic growth control Growth inhibition reflects upstream circadian and hormonal effects
7 Apoptosis sensitivity ↑ sensitivity to apoptosis (chemo/RT) ↓ apoptosis Phenotypic Therapy sensitization Melatonin enhances response to chemo- and radiotherapy while protecting normal tissue


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⟱
6419- MEL,    The potential influence of melatonin on mitochondrial quality control: a review
- Review, Nor, NA
*mt-ACC⇅, *PKM1↑, *PKM2↑, *Glycolysis↝, *PDKs↑, *FAO↑, *ETC↑, *OXPHOS↑, *ATP↑, Glycolysis↓, OXPHOS↑, *Ca+2↓, *ROS↓, *antiOx↑, *SOD2↑, *GPx↑, *Catalase↑, *MFN1↑, *MFN2↑, *OPA1↑, *YAP/TEAD↑, *Hippo↑, *SIRT1↑, *PGC-1α↑, *DRP1/DNM1L↓,

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

OXPHOS↑, 1,  

Core Metabolism/Glycolysis

Glycolysis↓, 1,  
Total Targets: 2

Pathway results for Effect on Normal Cells:


NA, unassigned

DRP1/DNM1L↓, 1,   MFN1↑, 1,   MFN2↑, 1,   OPA1↑, 1,  

Redox & Oxidative Stress

antiOx↑, 1,   Catalase↑, 1,   GPx↑, 1,   OXPHOS↑, 1,   ROS↓, 1,   SOD2↑, 1,  

Mitochondria & Bioenergetics

ATP↑, 1,   ETC↑, 1,   PGC-1α↑, 1,  

Core Metabolism/Glycolysis

mt-ACC⇅, 1,   FAO↑, 1,   Glycolysis↝, 1,   PDKs↑, 1,   PKM1↑, 1,   PKM2↑, 1,   SIRT1↑, 1,  

Cell Death

Hippo↑, 1,   YAP/TEAD↑, 1,  

Migration

Ca+2↓, 1,  
Total Targets: 23

Scientific Paper Hit Count for: FAO, Fatty Acid Oxidation
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#:122  Target#:1044  State#:%  Dir#:%
wNotes=0 sortOrder:rid,rpid

 

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