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⟱
932- BBR,    The short-term effects of berberine in the liver: Narrow margins between benefits and toxicity
- in-vivo, Nor, NA
*glucoNG↓, These results can be regarded as evidence that the direct inhibitory effects of berberine on gluconeogenesis
*Glycolysis↑,
*NH3↑, inhibited ammonia detoxification
*NADPH/NADP+↑,
*ATP↓,
*toxicity↑, narrow margin between the expected benefits and toxicity

1883- DCA,    In vivo metabolic response of glucose to dichloroacetate in humans
- Analysis, Var, NA
BG↓, Dichloroacetate (DCA), which is known to increase the rate of pyruvate oxidation, has been shown to lower plasma glucose concentrations in normal fasting subjects
glucoNG↓, These results suggest that DCA may decrease gluconeogenesis by limiting the availability of the precursor substrates lactate and alanine.

5800- MET,    Metformin as anticancer agent and adjuvant in cancer combination therapy: Current progress and future prospect
- Review, Var, NA
ChemoSen↑, Some combination therapy strategies including metformin combined with chemotherapy, radiotherapy, targeted therapy and immunotherapy have been proven to have more significant antitumor effects
RadioS↑,
Imm↑,
*AntiDiabetic↑, Metformin, the preferred glucose-lowering drug for patients with T2DM, is typically an adenosine monophosphate-activated protein kinase (AMPK) activator
*AMPK↑,
TumCP↓, AMPK restores the normal function of the liver and other tissues in diabetic patients as well as stops the metabolism of rapidly proliferating tumors
hepatoP↑,
ATP↓, . This leads to a decrease in intracellular ATP and an increase in AMP levels, which inhibits gluconeogenesis and further activates AMPK.
AMP↑,
glucoNG↓,
ROS↑, metformin can also promote reactive oxygen species (ROS) production by inhibiting mitochondrial respiratory-chain complex I, which can lead to DNA damage and gene mutation [23]
compI↓,
DNAdam↑,
CSCs↓, The advantage of metformin combined with chemotherapy is related to killing cancer stem cells [30].
NP/CIPN↓, metformin could improve the adverse effects of neuropathy (PN) in paclitaxel-treated breast cancer patients
chemoP↑, Thus, metformin may be able to be used as a chemoprotective agent, reducing the toxicity of chemotherapy and ameliorating adverse effects.
toxicity↓, The safety and tolerability of metformin were confirmed, but a large number of phase III clinical trials are still needed to follow up the study
Trx↓, Metformin radiosensitizes ductal breast cancer MCF7 cells by increasing intracellular reactive oxygen species (ROS) production through decreased thioredoxin (Trx) expression
eff↑, In addition, metformin may act in combination with the aspirin metabolite salicylic acid to enhance the proliferation inhibition of radiotherapy on prostate cancer
cycD1/CCND1↓, addition of metformin reduced the expression levels of cyclin D1, CDK4, CDK6, cyclin E, and CDK2 in gastric cancer cells
CDK4↓,
CDK6↓,
cycE/CCNE↓,
CDK2↓,

2493- MET,    Metformin Inhibits Gluconeogenesis by a Redox-Dependent Mechanism In Vivo
- in-vivo, Nor, NA
glucoNG↓, Metformin, the universal first-line treatment for type 2 diabetes, exerts its therapeutic glucose-lowering effects by inhibiting hepatic gluconeogenesis
glucose↓, metformin suppressed hepatic glucose production from gluconeogenic substrates that depend on cytosolic NADH (lactate and glycerol), but not from gluconeogenic substrates independent of cytosolic NADH

2492- MET,    The Metformin Mechanism on Gluconeogenesis and AMPK Activation: The Metabolite Perspective
- Review, Nor, NA
*glucose↓, Metformin therapy lowers blood glucose in type 2 diabetes by targeting various pathways including hepatic gluconeogenesis.
*glucoNG↓, inhibits gluconeogenesis
*AMPK↑, The activation of AMPK by metformin

2491- MET,    Metformin suppresses gluconeogenesis by inhibiting mitochondrial glycerophosphate dehydrogenase
- in-vivo, Nor, NA
*glucoNG↓, Metformin suppresses gluconeogenesis by inhibiting mitochondrial glycerophosphate dehydrogenase
*glucose↓, Acute and chronic low-dose metformin treatment effectively reduced endogenous glucose production (EGP)
*mitResp↓, These findings are supported by our data showing that metformin significantly inhibited mitochondrial respiration from G-3-P

2448- SFN,    Sulforaphane and bladder cancer: a potential novel antitumor compound
- Review, Bladder, NA
Apoptosis↑, Recent studies have demonstrated that Sulforaphane not only induces apoptosis and cell cycle arrest in BC cells, but also inhibits the growth, invasion, and metastasis of BC cells
TumCG↓,
TumCI↓,
TumMeta↓,
glucoNG↓, Additionally, it can inhibit BC gluconeogenesis
ChemoSen↑, demonstrate definite effects when combined with chemotherapeutic drugs/carcinogens.
TumCCA↑, SFN can block the cell cycle in G2/M phase, upregulate the expression of Caspase3/7 and PARP cleavage, and downregulate the expression of Survivin, EGFR and HER2/neu
Casp3↑,
Casp7↑,
cl‑PARP↑,
survivin↓,
EGFR↓,
HER2/EBBR2↓,
ATP↓, SFN inhibits the production of ATP by inhibiting glycolysis and mitochondrial oxidative phosphorylation in BC cells in a dose-dependent manner
Glycolysis↓,
mt-OXPHOS↓,
AKT1↓, dysregulation of glucose metabolism by inhibiting the AKT1-HK2 axis
HK2↓,
Hif1a↓, Sulforaphane inhibits glycolysis by down-regulating hypoxia-induced HIF-1α
ROS↑, SFN can upregulate ROS production and Nrf2 activity
NRF2↑,
EMT↓, inhibiting EMT process through Cox-2/MMP-2, 9/ ZEB1 and Snail and miR-200c/ZEB1 pathways
COX2↓,
MMP2↓,
MMP9↓,
Zeb1↓,
Snail↓,
HDAC↓, FN modulates the histone status in BC cells by regulating specific HDAC and HATs,
HATs↓,
MMP↓, SFN upregulates ROS production, induces mitochondrial oxidative damage, mitochondrial membrane potential depolarization, cytochrome c release
Cyt‑c↓,
Shh↓, SFN significantly lowers the expression of key components of the SHH pathway (Shh, Smo, and Gli1) and inhibits tumor sphere formation, thereby suppressing the stemness of cancer cells
Smo↓,
Gli1↓,
BioAv↝, SFN is unstable in aqueous solutions and at high temperatures, sensitive to oxygen, heat and alkaline conditions, with a decrease in quantity of 20% after cooking, 36% after frying, and 88% after boiling
BioAv↝, It has been reported that the ability of individuals to use gut myrosinase to convert glucoraphanin into SFN varies widely
Dose↝, Excitingly, it has been reported that daily oral administration of 200 μM SFN in melanoma patients can achieve plasma levels of 655 ng/mL with good tolerance


Showing Research Papers: 1 to 7 of 7

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 7

Pathway results for Effect on Cancer / Diseased Cells:


Redox & Oxidative Stress ⓘ

compI↓, 1,   NRF2↑, 1,   mt-OXPHOS↓, 1,   ROS↑, 2,   Trx↓, 1,  

Mitochondria & Bioenergetics ⓘ

ATP↓, 2,   MMP↓, 1,  

Core Metabolism/Glycolysis ⓘ

AKT1↓, 1,   AMP↑, 1,   glucoNG↓, 4,   glucose↓, 1,   Glycolysis↓, 1,   HK2↓, 1,  

Cell Death ⓘ

Apoptosis↑, 1,   Casp3↑, 1,   Casp7↑, 1,   Cyt‑c↓, 1,   survivin↓, 1,  

Kinase & Signal Transduction ⓘ

HER2/EBBR2↓, 1,  

Transcription & Epigenetics ⓘ

HATs↓, 1,  

DNA Damage & Repair ⓘ

DNAdam↑, 1,   cl‑PARP↑, 1,  

Cell Cycle & Senescence ⓘ

CDK2↓, 1,   CDK4↓, 1,   cycD1/CCND1↓, 1,   cycE/CCNE↓, 1,   TumCCA↑, 1,  

Proliferation, Differentiation & Cell State ⓘ

CSCs↓, 1,   EMT↓, 1,   Gli1↓, 1,   HDAC↓, 1,   Shh↓, 1,   Smo↓, 1,   TumCG↓, 1,  

Migration ⓘ

MMP2↓, 1,   MMP9↓, 1,   Snail↓, 1,   TumCI↓, 1,   TumCP↓, 1,   TumMeta↓, 1,   Zeb1↓, 1,  

Angiogenesis & Vasculature ⓘ

EGFR↓, 1,   Hif1a↓, 1,  

Immune & Inflammatory Signaling ⓘ

COX2↓, 1,   Imm↑, 1,  

Hormonal & Nuclear Receptors ⓘ

CDK6↓, 1,  

Drug Metabolism & Resistance ⓘ

BioAv↝, 2,   ChemoSen↑, 2,   Dose↝, 1,   eff↑, 1,   RadioS↑, 1,  

Clinical Biomarkers ⓘ

BG↓, 1,   EGFR↓, 1,   HER2/EBBR2↓, 1,  

Functional Outcomes ⓘ

chemoP↑, 1,   hepatoP↑, 1,   NP/CIPN↓, 1,   toxicity↓, 1,  
Total Targets: 58

Pathway results for Effect on Normal Cells:


Redox & Oxidative Stress ⓘ

NADPH/NADP+↑, 1,  

Mitochondria & Bioenergetics ⓘ

ATP↓, 1,   mitResp↓, 1,  

Core Metabolism/Glycolysis ⓘ

AMPK↑, 2,   glucoNG↓, 3,   glucose↓, 2,   Glycolysis↑, 1,   NH3↑, 1,  

Functional Outcomes ⓘ

AntiDiabetic↑, 1,   toxicity↑, 1,  
Total Targets: 10

Scientific Paper Hit Count for: glucoNG, gluconeogenesis
4 Metformin
1 Berberine
1 Dichloroacetate
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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