CPT1A Cancer Research Results

CPT1A, Carnitine Palmitoyltransferase 1A: Click to Expand ⟱
Source:
Type:
Carnitine Palmitoyltransferase 1A (CPT1A) is an enzyme that plays a crucial role in the regulation of fatty acid metabolism, particularly in the transport of long-chain fatty acids into mitochondria for beta-oxidation. In cancer, CPT1A has been implicated in the regulation of tumor cell metabolism, proliferation, and survival.

CPT1A typically overexpressed and is associated with poor prognosis and reduced overall survival in breast, lung, and colon cancers.
CPT1A expression is also associated with increased risk of metastasis and recurrence in various types of cancer.
Scientific Papers found: Click to Expand⟱
1172- Ash,    Withaferin A Inhibits Fatty Acid Synthesis in Rat Mammary Tumors
- in-vitro, BC, MCF-7 - in-vitro, BC, MDA-MB-231 - in-vivo, NA, NA
FASN↓,
ACLY↓,
ACC1↓,
CPT1A↓, FASN and CPT1A proteins were also decreased significantly upon WA treatment
SREBP1↓,

2740- BetA,    Effects and mechanisms of fatty acid metabolism-mediated glycolysis regulated by betulinic acid-loaded nanoliposomes in colorectal cancer
- in-vitro, CRC, HCT116
TumCP↓, BA-NLs significantly suppressed the proliferation and glucose uptake of CRC cells by regulating potential glycolysis and fatty acid metabolism targets and pathways, which forms the basis of the anti-CRC function of BA-NLs.
Glycolysis↓,
HK2↓, HK2, PFK-1, PEP and PK isoenzyme M2 (PKM2) in glycolysis, and of ACSL1, CPT1a and PEP in fatty acid metabolism, were blocked by BA-NLs, which play key roles in the inhibition of glycolysis and fatty acid-mediated production of pyruvate and lactate.
PFK1↓,
PKM2↓,
ACSL1↓,
CPT1A↓,
FASN↓,
FAO↓, Significant reduction of FAO was detected in BA-NL-treated HCT116 cells
GlucoseCon↓, glucose uptake in HCT116 cells was significantly decreased by BA-NLs
lactateProd↓, lactic acid secretion was significantly suppressed in HCT116 cells treated with BA-NLs

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 4 of 4

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 4

Pathway results for Effect on Cancer / Diseased Cells:


Redox & Oxidative Stress ⓘ

ROS↓, 1,  

Mitochondria & Bioenergetics ⓘ

SDH↓, 1,  

Core Metabolism/Glycolysis ⓘ

ACC1↓, 2,   ACLY↓, 1,   ACSL1↓, 1,   citrate↓, 1,   CPT1A↓, 4,   FAO↓, 1,   FASN↓, 3,   FASN↑, 1,   GlucoseCon↓, 1,   Glycolysis↓, 3,   HK2↓, 3,   lactateProd↓, 1,   LDHA↓, 1,   PDH↓, 1,   PFK1↓, 1,   PFK2?, 1,   PKM2↓, 3,   SREBP1?, 1,   SREBP1↓, 1,   TCA↓, 1,   β-oxidation↓, 2,  

Cell Death ⓘ

Casp2↑, 1,   Casp3↑, 1,   Casp8↑, 1,   Casp9↑, 1,   Mcl-1↓, 1,  

DNA Damage & Repair ⓘ

cl‑PARP↑, 1,  

Proliferation, Differentiation & Cell State ⓘ

IGF-1R↓, 1,   PTEN↑, 1,  

Migration ⓘ

Ca+2↓, 1,   TumCP↓, 1,  

Angiogenesis & Vasculature ⓘ

angioG↓, 1,   Hif1a↓, 1,  

Barriers & Transport ⓘ

GLUT1↓, 1,  

Immune & Inflammatory Signaling ⓘ

T-Cell↝, 1,  

Drug Metabolism & Resistance ⓘ

Dose↓, 1,   Dose∅, 1,   eff↓, 1,   eff↑, 5,  
Total Targets: 41

Pathway results for Effect on Normal Cells:


Total Targets: 0

Scientific Paper Hit Count for: CPT1A, Carnitine Palmitoyltransferase 1A
1 Ashwagandha(Withaferin A)
1 Betulinic acid
1 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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