FASN Cancer Research Results

FASN, Fatty acid synthase: Click to Expand ⟱
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Type:
Fatty acid synthase (FASN) is an enzyme involved in the synthesis of fatty acids, which are essential for cell growth and proliferation. Overexpression of FASN has been observed in various types of cancer, and it is often associated with poor prognosis.
-fatty acid synthase (FAS) has been demonstrated to play an important role in carcinogenesis by protecting cells from apoptosis

FASN (fatty acid synthase) is a key enzyme in the de novo synthesis of fatty acids and has been widely studied in cancer due to its role in lipid metabolism and energy production. Altered FASN expression has been reported in various malignancies, and its prognostic implications have been explored across several tumor types.

FASN is frequently overexpressed in a variety of cancers, including breast, prostate, colorectal, ovarian, and others.
• Many cancers require high levels of fatty acid synthesis for the generation of new membranes and for signaling lipid molecules.
• Higher FASN expression is generally associated with more aggressive cancer phenotypes, increased metastatic potential, and poorer patient outcomes.
• Its role in promoting de novo fatty acid synthesis links it directly to the metabolic demands of rapidly dividing cancer cells, making it both a prognostic biomarker and a promising therapeutic target.
Scientific Papers found: Click to Expand⟱
1578- Citrate,    Understanding the Central Role of Citrate in the Metabolism of Cancer Cells and Tumors: An Update
- Review, Var, NA
TCA↑,
FASN↑, Cytosolic acetyl-CoA sustains fatty acid (FA) synthesis (FAS)
Glycolysis↓,
glucoNG↑, while it enhances gluconeogenesis by promoting fructose-1,6-biphosphatase (FBPase)
PFK1↓, citrate directly inhibits the main regulators of glycolysis, phosphofructokinase-1 (PFK1) and phosphofructokinase-2 (PFK2)
PFK2↓, well-known inhibitor of PFK
FBPase↑, enhances gluconeogenesis by promoting fructose-1,6-biphosphatase (FBPase)
TumCP↓, inhibits the proliferation of various cancer cells of solid tumors (human mesothelioma, gastric and ovarian cancer cells) at high concentrations (10–20 mM),
eff↑, promoting apoptosis and the sensitization of cells to cisplatin
ACLY↓, higher concentrations (10 mM or more) decreased both acetylation and ACLY expression
Dose↑, In various cell lines, a high concentration of citrate—generally above 10 mM—inhibits the proliferation of cancer cells in a dose dependent manner
Casp3↑,
Casp2↑,
Casp8↑,
Casp9↑,
Bcl-xL↓,
Mcl-1↓,
IGF-1R↓, citrate at high concentration (10 mM) also inhibits the insulin-like growth factor-1 receptor (IGF-1R)
PI3K↓, pathways
Akt↓, activates PTEN, the key phosphatase inhibiting the PI3K/Akt pathway
mTOR↓,
PTEN↑, high dose of citrate activates PTEN
ChemoSen↑, citrate increases the sensibility of cells to chemotherapy (in particular, cisplatin)
Dose?, oral gavage of citrate sodium (4 g/kg twice a day) for several weeks (4 to 7 weeks) significantly regressed tumors

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.

3094- RES,    Resveratrol suppresses growth of cancer stem-like cells by inhibiting fatty acid synthase
- in-vitro, BC, MCF-7 - in-vitro, BC, MDA-MB-231
CSCs↓, resveratrol significantly reduced the cell viability and mammosphere formation followed by inducing apoptosis in cancer stem-like cells
tumCV↓,
FASN↑, This inhibitory effect of resveratrol is accompanied by a significant reduction in lipid synthesis which is caused by the down-regulation of the fatty acid synthase (FAS) gene
BNIP3↑, followed by up-regulation of pro-apoptotic genes, DAPK2 and BNIP3.
*cardioP↑, cardio-protective effect of resveratrol has been extensively studied in various pre-clinical models, and it has been shown that the strong anti-oxidant activity of resveratrol
*antiOx↑,
NF-kB↓, down-regulation of NF-kappaB, COX and matrix metalloprotease-9 (MMP9) expression
COX2↓,
MMP9↓,
IGF-1↓, resveratrol as diet significantly reduced the onset of prostate cancer and exhibited a decrease in IGF1 (insulin-like growth factor 1) and phosphorylated-ERK1 (extracellular regulating kinase 1)
ERK↓,
lipid-P↓, resveratrol is indeed capable of suppressing lipid metabolism by blocking the FAS expression followed by induction of apoptosis in cancer stem-like cells
CD24↓, Resveratrol induces apoptosis in tumor stem-like cells by suppressing FAS (we first isolated cancer stem-like cells (CD24-/CD44+/ESA+) from MDA-MB231)


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 ⓘ

lipid-P↓, 1,   ROS↓, 1,  

Mitochondria & Bioenergetics ⓘ

SDH↓, 1,  

Core Metabolism/Glycolysis ⓘ

ACLY↓, 1,   citrate↓, 1,   CPT1A↓, 1,   FASN↑, 3,   FBPase↑, 1,   glucoNG↑, 1,   Glycolysis↓, 2,   HK2↓, 1,   PDH↓, 1,   PFK1↓, 1,   PFK2?, 1,   PFK2↓, 1,   PKM2↓, 1,   TCA↓, 1,   TCA↑, 1,   β-oxidation↓, 1,  

Cell Death ⓘ

Akt↓, 1,   Bcl-xL↓, 1,   Casp2↑, 2,   Casp3↑, 2,   Casp8↑, 2,   Casp9↑, 2,   Mcl-1↓, 2,  

Transcription & Epigenetics ⓘ

tumCV↓, 1,  

Autophagy & Lysosomes ⓘ

BNIP3↑, 1,  

DNA Damage & Repair ⓘ

cl‑PARP↑, 1,  

Proliferation, Differentiation & Cell State ⓘ

CD24↓, 1,   CSCs↓, 1,   ERK↓, 1,   IGF-1↓, 1,   IGF-1R↓, 2,   mTOR↓, 1,   PI3K↓, 1,   PTEN↑, 2,  

Migration ⓘ

Ca+2↓, 1,   MMP9↓, 1,   TumCP↓, 1,  

Angiogenesis & Vasculature ⓘ

angioG↓, 1,   Hif1a↓, 1,  

Barriers & Transport ⓘ

GLUT1↓, 1,  

Immune & Inflammatory Signaling ⓘ

COX2↓, 1,   NF-kB↓, 1,   T-Cell↝, 1,  

Drug Metabolism & Resistance ⓘ

ChemoSen↑, 1,   Dose?, 1,   Dose↓, 1,   Dose↑, 1,   Dose∅, 1,   eff↓, 1,   eff↑, 6,  
Total Targets: 53

Pathway results for Effect on Normal Cells:


Redox & Oxidative Stress ⓘ

antiOx↑, 1,  

Functional Outcomes ⓘ

cardioP↑, 1,  
Total Targets: 2

Scientific Paper Hit Count for: FASN, Fatty acid synthase
2 Citric Acid
1 Resveratrol
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#:931  State#:%  Dir#:2
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