β-oxidation Cancer Research Results

β-oxidation, Beta Oxidation: Click to Expand ⟱
Source:
Type:
Beta-oxidation serves as a major pathway for breaking down fatty acids into acetyl-CoA, which then enters the tricarboxylic acid (TCA) cycle to generate ATP.

– In tumors with limited glucose availability or under metabolic stress, enhanced fatty acid oxidation can serve as an alternative energy source, supporting cell survival and proliferation.
– Beta-oxidation contributes to the removal of excess fatty acids and provides substrates for oxidative phosphorylation, thereby influencing the balance between energy production and biosynthetic needs.
– Tumor environments are often hypoxic and nutrient-deprived. Enhanced beta-oxidation can allow cancer cells to adapt by optimizing energy yield from available substrates.

– Upregulated beta-oxidation or reliance on fatty acid metabolism in certain tumors has been correlated with increased aggressiveness, metastasis, and a poor overall prognosis.
Pca, Prostate Cancer: Click to Expand ⟱
Prostate Cancer: Alterations in genes such as ERG, SPOP, MYC, androgen receptor (AR), and CHD1, drive PCa progression.
TP53 is the most commonly mutated gene in human cancer.
HH↑, GLI-1↑, SHH↑ P53↓
The loss of p53 and/or other tumor suppressor genes, reduced capacity for DNA repair, the dysfunction of telomerase activity, and changes in the pathways that govern the growth of cells also mediate the progression of Pca.
It has been well documented that Ca2+ influx and MDR1 upregulation are highly associated with GEM metabolism in human pancreatic carcinoma.
Increased Growth factor IGF-1/IGF-1R axis activation mediated by both PI3K/Akt or RAF/MEK/ERK system and AR expression remains important in the development and progression of prostate cancer.
It has been demonstrated that prostate cancer cells are relatively sensitive to heat stress.
Long non-coding RNA MALAT1 has been reported as an oncogenic target in multiple types of cancers, including PC.
Scientific Papers found: Click to Expand⟱
2404- SFN,    Prostate cancer chemoprevention by sulforaphane in a preclinical mouse model is associated with inhibition of fatty acid metabolism
- in-vitro, Pca, LNCaP - in-vitro, Pca, 22Rv1 - in-vivo, NA, NA
ACC1↓, FASN↓, CPT1A↓, β-oxidation↓, SREBP1?, HK2↓, PKM2↓, LDHA↓, Glycolysis↓,

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:


Core Metabolism/Glycolysis ⓘ

ACC1↓, 1,   CPT1A↓, 1,   FASN↓, 1,   Glycolysis↓, 1,   HK2↓, 1,   LDHA↓, 1,   PKM2↓, 1,   SREBP1?, 1,   β-oxidation↓, 1,  
Total Targets: 9

Pathway results for Effect on Normal Cells:


Total Targets: 0

Scientific Paper Hit Count for: β-oxidation, Beta 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:22  Cells:%  prod#:%  Target#:1145  State#:%  Dir#:1
  wNotes=0  sortOrder:rid,rpid

 

Home Page