FAM Cancer Research Results

FAM, Fatty Acid Metabolism: Click to Expand ⟱
Source:
Type:

Fatty Acid Metabolism - Fatty Acid Synthesis, Uptake, Transport, and Oxidation

Type: Metabolic pathway / lipid metabolism pathway

Function: Fatty acid metabolism encompasses the uptake, intracellular transport, de novo synthesis, elongation, desaturation, storage, mobilization, and mitochondrial or peroxisomal oxidation of fatty acids. Major regulatory components include SREBP-1/SREBF1, ACLY, ACACA/ACC, FASN, SCD, FABPs, CD36, ACSL enzymes, CPT1, and enzymes of mitochondrial β-oxidation. The pathway supplies membrane lipids, signaling molecules, ATP, reducing equivalents, and metabolic intermediates.

Cancer: ↑ / reprogrammed. Cancer cells frequently increase fatty-acid uptake, de novo lipogenesis, and/or fatty-acid oxidation to meet demands for membrane synthesis, energy production, redox homeostasis, survival, and signaling. Altered fatty-acid metabolism can promote proliferation, cancer stemness, invasion, metastasis, immune evasion, ferroptosis resistance, and treatment resistance. The dominant branch varies by tumor type and metabolic environment.

Alzheimer's Disease: ↕ Dysregulated. Alzheimer's disease is associated with altered fatty-acid composition, polyunsaturated fatty-acid metabolism, lipid transport, mitochondrial fatty-acid utilization, and membrane lipid homeostasis. These abnormalities can influence mitochondrial function, amyloid-β metabolism, tau pathology, neuroinflammation, synaptic function, and oxidative stress. Because individual fatty acids and metabolic branches may change in opposite directions, a single increase or decrease does not adequately describe the pathway.
Scientific Papers found: Click to Expand⟱
7757- ISL,    Isoliquiritigenin Suppresses Oral Squamous Cell Carcinoma Progression by Targeting FABP5-Mediated Lipid Metabolism: Association with the circPOLB/miR-548ae-3p/C-MYC Axis
- in-vitro, Oral, NA
FABP5/E-FABP↓, FAM↓, TumCI↓, lipidLev↓,
7779- ISL,    Isoliquiritigenin-mediated miR-23a-3p inhibition activates PGC-1α to alleviate alcoholic liver injury
- in-vivo, Alcohol, NA
*hepatoP↑, *FAM↑, *PGC-1α↑, *PPARα↑, *CPT1A↑, *ACADS/SCAD↑, *ROS↓, *TNF-α↓, *IL1β↓, *IL6↓, *miR-23a-3p↓,

Showing Research Papers: 1 to 2 of 2

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 2

Pathway results for Effect on Cancer / Diseased Cells:


NA, unassigned(tgid=0) ⓘ

FABP5/E-FABP↓, 1,   FAM↓, 1,  

Core Metabolism/Glycolysis(tgid=4) ⓘ

lipidLev↓, 1,  

Migration(tgid=13) ⓘ

TumCI↓, 1,  
Total Targets: 4

Pathway results for Effect on Normal Cells:


NA, unassigned(tgid=0) ⓘ

ACADS/SCAD↑, 1,   FAM↑, 1,   miR-23a-3p↓, 1,  

Redox & Oxidative Stress(tgid=1) ⓘ

ROS↓, 1,  

Mitochondria & Bioenergetics(tgid=3) ⓘ

PGC-1α↑, 1,  

Core Metabolism/Glycolysis(tgid=4) ⓘ

CPT1A↑, 1,   PPARα↑, 1,  

Immune & Inflammatory Signaling(tgid=16) ⓘ

IL1β↓, 1,   IL6↓, 1,   TNF-α↓, 1,  

Clinical Biomarkers(tgid=22) ⓘ

IL6↓, 1,  

Functional Outcomes(tgid=23) ⓘ

hepatoP↑, 1,  
Total Targets: 12

Scientific Paper Hit Count for: FAM, Fatty Acid Metabolism
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#:1693  State#:%  Dir#:%
  wNotes=0  sortOrder:rid,rpid

 

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