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.
Scientific Papers found: Click to Expand⟱
1593- Citrate,    Citrate Induces Apoptotic Cell Death: A Promising Way to Treat Gastric Carcinoma?
- in-vitro, GC, BGC-823 - in-vitro, GC, SGC-7901
PFK↓, citrate, a strong physiological inhibitor of phosphofructokinase (PFK)
Glycolysis↓, citrate is a strong inhibitor of glycolysis
tumCV↓, 10 mM citrate led to a nearly complete disappearance of cancer cells, and after 72 h, no cells remained viable whatever the concentration used
cl‑Casp3↑,
cl‑PARP↑,
Apoptosis↑,
ATP↓, depletion of ATP generated by citrate
ChemoSen↑, In the previous study, citrate sensitized the cells to cisplatin, a drug which was poorly efficient by itself on such cells
Mcl-1↓, In the current study, citrate reduced MCL-1 expression in both the gastric cancer lines in a dose-dependent manner, in agreement with previous observations in mesothelioma cells
glucoNG↑, citrate activates neoglucogenesis by enhancing fructose 1,6-bisphosphatase activity
FBPase↑,
OXPHOS↓, When citrate is abundant in cells, this usually means that energy production (ATP) is sufficient, so oxidative phosphorylation (OXPHOS) and the Krebs cycle are slowed down or stopped.
TCA↓, Krebs cycle are slowed down or stopped.
β-oxidation↓, concomitantly inhibits β-oxidation
HK2↓, It may inhibit HK, at least indirectly, by the physiological retroaction of glucose-6-phosphate (G6P) on HK
PDH↓, citrate may inhibit pyruvate dehydrogenase (PDH) (39), the enzyme of the Krebs cycle which links glycolysis and the tricarboxylic cycle
ROS↑, citrate could also promote the formation of reactive oxygen species (ROS) since a sudden elevation of citrate concentration inside the cell might immediately stimulate the Krebs cycle.

1576- Citrate,    Targeting citrate as a novel therapeutic strategy in cancer treatment
- Review, Var, NA
TCA↓, Citrate serves as a key metabolite in the tricarboxylic acid cycle (TCA cycle, also referred to as the Krebs cycle)
T-Cell↝, modulation of T cell differentiation
Glycolysis↓, Citrate directly suppresses both cell glycolysis and TCA.
PKM2↓, citrate also inhibits glycolysis via its indirect inhibition of PK
PFK2?, In addition, citrate can inhibit PFK2,
SDH↓, citrate can inhibit enzymes, such as succinate dehydrogenase (SDH) and pyruvate dehydrogenase (PDH), in the TCA cycle
PDH↓,
β-oxidation↓, Citrate also inhibits β-oxidation as it promotes the formation of malonyl-CoA, which decreases the mitochondrial transport of fatty acids by inhibiting carnitine palmitoyl transferase I (CPT I)
CPT1A↓,
FASN↑, citrate has a positive role in promoting fatty acid synthesis
Casp3↑,
Casp2↑,
Casp8↑,
Casp9↑,
cl‑PARP↑,
Hif1a↓, Notably, in AML cell line U937, citrate induces apoptosis in a dose- and time-dependent manner by regulating the expression of HIF-1α and its downstream target GLUT-1
GLUT1↓,
angioG↓, citrate can also inhibit angiogenesis
Ca+2↓, chelate calcium ions in tumor cells
ROS↓, The other potential mechanism involved in citrate-mediated promotion of cancer growth and proliferation may be through its ability to decrease the levels of reactive oxygen species (ROS) in tumor cells
eff↓, dual effects of citrate in tumors may depend on the concentrations of citrate treatment, and different concentrations may bring out completely opposite effects even in the same tumor.
Dose↓, citrate concentration (<5 mM) appears to boost tumor growth and expansion in lung cancer A549 cells. 10mM and higher inhibited cell growth.
eff↑, citrate combined with ultraviolet (UV) radiation caused activation of caspase-3 and -9 in tumor cells (
Mcl-1↓, citrate has also been found to downregulate Mcl-1
HK2↓, Citrate also inhibits the enzymes PFK1 and hexokinase II (HK II) in glycolysis in tumor cells
IGF-1R↓,
PTEN↑, citrate may exert its effect via activating PTEN pathway
citrate↓, In addition to prostate cancer, citrate levels are significantly decreased in blood of patients with lung, bladder, pancreas and esophagus cancers
Dose∅, daily oral administration of citrate for 7 weeks at dose of 4 g/kg/day reduces tumor growth of several xenograft tumors and increases significantly the numbers of tumor-infiltrating T cells with no significant side effects in mouse models
eff↑, combining citrate with other compounds such as celecoxib, cisplatin, and 3-bromo-pyruvate, and have generated promising results
eff↑, combination of low effective doses of 3-bromo-pyruvate (3BP) (15uM), an inhibitor of glycolysis, and citrate (3 mM) significantly depleted the proliferation capability and migratory power of the C6 glioma
eff↑, Zinc treatment could lead to citrate accumulation in malignant prostate cells, which could have therapeutic potential in clinical therapy of prostate cancer.
eff↑, synergistic efficacy mediated by citrate combined with current checkpoint blockade therapies with anti-CTLA4 and/or anti-PD1/PDL1 will develop alternative novel strategies for future immunotherapy.

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↓, SFN (5 and 10 μM) resulted in downregulation of protein and mRNA levels of acetyl-CoA carboxylase 1 (ACC1) and fatty acid synthase (FASN), but not ATP citrate lyase
FASN↓,
CPT1A↓, SFN decreased ACC1, FASN and CPT1A expression in LNCaP and 22Rv1 cells
β-oxidation↓, SFN treatment decreased expression of β-oxidation dehydrogenases
SREBP1?, SFN treatment decreased SREBP1 protein level in prostate cancer cells
HK2↓, Similarly, when Hi-Myc mice were given 1 mg/mouse of sulforaphane three times each week for 5–10 weeks, expression of HKII, PKM2 and LDHA was significantly decreased.
PKM2↓,
LDHA↓,
Glycolysis↓, These results provide evidence that sulforaphane suppresses in vivo glycolysis in prostate cancer cells


Showing Research Papers: 1 to 3 of 3

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 3

Pathway results for Effect on Cancer / Diseased Cells:


Redox & Oxidative Stress ⓘ

OXPHOS↓, 1,   ROS↓, 1,   ROS↑, 1,  

Mitochondria & Bioenergetics ⓘ

ATP↓, 1,   SDH↓, 1,  

Core Metabolism/Glycolysis ⓘ

ACC1↓, 1,   citrate↓, 1,   CPT1A↓, 2,   FASN↓, 1,   FASN↑, 1,   FBPase↑, 1,   glucoNG↑, 1,   Glycolysis↓, 3,   HK2↓, 3,   LDHA↓, 1,   PDH↓, 2,   PFK↓, 1,   PFK2?, 1,   PKM2↓, 2,   SREBP1?, 1,   TCA↓, 2,   β-oxidation↓, 3,  

Cell Death ⓘ

Apoptosis↑, 1,   Casp2↑, 1,   Casp3↑, 1,   cl‑Casp3↑, 1,   Casp8↑, 1,   Casp9↑, 1,   Mcl-1↓, 2,  

Transcription & Epigenetics ⓘ

tumCV↓, 1,  

DNA Damage & Repair ⓘ

cl‑PARP↑, 2,  

Proliferation, Differentiation & Cell State ⓘ

IGF-1R↓, 1,   PTEN↑, 1,  

Migration ⓘ

Ca+2↓, 1,  

Angiogenesis & Vasculature ⓘ

angioG↓, 1,   Hif1a↓, 1,  

Barriers & Transport ⓘ

GLUT1↓, 1,  

Immune & Inflammatory Signaling ⓘ

T-Cell↝, 1,  

Drug Metabolism & Resistance ⓘ

ChemoSen↑, 1,   Dose↓, 1,   Dose∅, 1,   eff↓, 1,   eff↑, 5,  
Total Targets: 43

Pathway results for Effect on Normal Cells:


Total Targets: 0

Scientific Paper Hit Count for: β-oxidation, Beta Oxidation
2 Citric Acid
1 Sulforaphane (mainly Broccoli)
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

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