glucoNG Cancer Research Results

glucoNG, gluconeogenesis: Click to Expand ⟱
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Gluconeogenesis is the metabolic pathway through which organisms synthesize glucose from non-carbohydrate precursors. This process is crucial for maintaining blood glucose levels, especially during fasting or intense exercise. In the context of cancer, gluconeogenesis can play a significant role in tumor metabolism and growth.
Cancer cells often exhibit altered metabolic pathways, a phenomenon known as the Warburg effect, where they preferentially use glycolysis for energy production even in the presence of oxygen. However, gluconeogenesis can also be upregulated in certain cancer types, providing a source of glucose to support rapid cell proliferation.
Cancer cells can utilize various substrates for gluconeogenesis, including lactate, amino acids (especially alanine and glutamine), and glycerol. This allows tumors to generate glucose even when dietary glucose is limited.
Hormones such as glucagon and cortisol can stimulate gluconeogenesis. In cancer, the dysregulation of these hormones can contribute to altered glucose metabolism.
Key Enzymes in Gluconeogenesis
Pyruvate Carboxylase (PC)
Phosphoenolpyruvate Carboxykinase (PEPCK)
Fructose-1,6-bisphosphatase (FBPase)
Glucose-6-phosphatase (G6Pase)

The expression of gluconeogenic enzymes is often altered in various cancers, and their upregulation is generally associated with poorer 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.

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


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:


Redox & Oxidative Stress ⓘ

OXPHOS↓, 1,   ROS↑, 1,  

Mitochondria & Bioenergetics ⓘ

ATP↓, 1,  

Core Metabolism/Glycolysis ⓘ

ACLY↓, 1,   FASN↑, 1,   FBPase↑, 2,   glucoNG↑, 2,   Glycolysis↓, 2,   HK2↓, 1,   PDH↓, 1,   PFK↓, 1,   PFK1↓, 1,   PFK2↓, 1,   TCA↓, 1,   TCA↑, 1,   β-oxidation↓, 1,  

Cell Death ⓘ

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

Transcription & Epigenetics ⓘ

tumCV↓, 1,  

DNA Damage & Repair ⓘ

cl‑PARP↑, 1,  

Proliferation, Differentiation & Cell State ⓘ

IGF-1R↓, 1,   mTOR↓, 1,   PI3K↓, 1,   PTEN↑, 1,  

Migration ⓘ

TumCP↓, 1,  

Drug Metabolism & Resistance ⓘ

ChemoSen↑, 2,   Dose?, 1,   Dose↑, 1,   eff↑, 1,  
Total Targets: 36

Pathway results for Effect on Normal Cells:


Total Targets: 0

Scientific Paper Hit Count for: glucoNG, gluconeogenesis
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#:126  State#:%  Dir#:2
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