G6PD Cancer Research Results

G6PD, Glucose-6-phosphate dehydrogenase: Click to Expand ⟱
Source:
Type:
Glucose-6-phosphate dehydrogenase (G6PD) is an enzyme that plays a crucial role in the pentose phosphate pathway (PPP), a metabolic pathway that generates NADPH and pentoses from glucose-6-phosphate. G6PD is the first enzyme in the PPP and is responsible for catalyzing the conversion of glucose-6-phosphate to 6-phosphogluconate, producing NADPH in the process.
**** patients who receive intravenous ascorbate must be prescreened for glucose 6 phosphate dehydrogenase deficiency.

G6PD expression is often elevated in various cancers and is generally linked to poorer prognosis.
Scientific Papers found: Click to Expand⟱
3100- RES,    Neuroprotective effects of resveratrol in Alzheimer disease pathology
- Review, AD, NA
*neuroP↑, several studies have reported interesting insights about the neuroprotective properties of the polyphenolic compound resveratrol
*BioAv↓, However, resveratrol’s low bioavailability originating from its poor water solubility and resulting from its short biological half-life
*Half-Life↓,
*BioAv↑, encapsulation in liposomal formulations
*BBB↑, Resveratrol being a lipophilic compound can readily cross the BBB via transmembrane diffusion
*NRF2↑, resveratrol into aged cells leading to the activation of cellular Nrf2-mediated antioxidant defense systems
*BioAv↓, An oral dose of 25 mg results in less than 5 μg/mL in the serum following absorption through the gastrointestinal tract, corresponding to approximately a 1000-fold decrease in bioavailability.
*BioAv↑, Treatment with pterostilbene also produced a sevenfold rise in its oral bioavailability than the parent resveratrol
*SIRT1↑, Amongst all the naturally occurring activators of SIRT 1, resveratrol is considered to be the most effective SIRT 1 activator.
*cognitive↑, Pterostilbene has shown to be a potent modulator of cognition and cellular oxidative stress associated with AD
*lipid-P↓, Figure 2
*HO-1↑,
*SOD↑,
*GSH↑,
*GPx↑,
*G6PD↑,
*PPARγ↑,
*AMPK↑,
*Aβ↓, Lowered Aβ levels by activating AMPK pathway

2444- SFN,    Sulforaphane Delays Fibroblast Senescence by Curbing Cellular Glucose Uptake, Increased Glycolysis, and Oxidative Damage
- in-vitro, Nor, MRC-5
*GlucoseCon↓, SFN delayed senescence by decreasing glucose metabolism on the approach to senescence, exhibiting a caloric restriction mimetic-like activity
*ROS↓, and thereby decreased oxidative damage to cell protein and DNA
*Trx↓, This was associated with increased expression of thioredoxin-interacting protein, curbing entry of glucose into cells;
*HK2↓, decreased hexokinase-2
*NRF2↑, SFN is an activator of transcription factor Nrf2 [14] which regulates antioxidant response element- (ARE-) linked gene expression.
*Catalase↑, CAT, PDRX1, and GCLM, expression was increased in senescence and treatment with SFN increased the expression further
*TXNIP↑, increased expression of TXNIP, curbing the entry of glucose into cells
*PFKFB2↓, decreased PFKFB2 and increased G6PD, downregulating glycolysis.
*G6PD↑,

4330- VitB5,    Metabolic changes and inflammation in cultured astrocytes from the 5xFAD mouse model of Alzheimer’s disease: Alleviation by pantethine
- in-vivo, AD, NA
*neuroP↑, Pantethine, the vitamin B5 precursor, known to be neuroprotective and anti-inflammatory, alleviated the pathological pattern in Tg astrocytes
*Inflam↓, pantethine has anti-inflammatory properties,
*ATP↑, Importantly, ATP had its levels increased by 44% in pantethine-treated Tg astrocytes compared to untreated.
*G6PD↑, Pantethine treatment increased both G6PD and PK activity in WT by about 40% and 25%, respectively.
*NADPH↑, in agreement, astrocyte NADPH levels paralleled the changes of G6PD activity described above
*IL1β↓, Pantethine treatment significantly reduced both IL-1β mRNA and protein expression in all conditions where it was applied
*other↝, Administered, at the right time during the disease progression, the pleiotropic action of this natural compound could therefore bring improvement in a complex pathological situation such as AD.


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:


Total Targets: 0

Pathway results for Effect on Normal Cells:


Redox & Oxidative Stress ⓘ

Catalase↑, 1,   GPx↑, 1,   GSH↑, 1,   HO-1↑, 1,   lipid-P↓, 1,   NRF2↑, 2,   ROS↓, 1,   SOD↑, 1,   Trx↓, 1,  

Mitochondria & Bioenergetics ⓘ

ATP↑, 1,  

Core Metabolism/Glycolysis ⓘ

AMPK↑, 1,   G6PD↑, 3,   GlucoseCon↓, 1,   HK2↓, 1,   NADPH↑, 1,   PFKFB2↓, 1,   PPARγ↑, 1,   SIRT1↑, 1,  

Transcription & Epigenetics ⓘ

other↝, 1,  

Migration ⓘ

TXNIP↑, 1,  

Barriers & Transport ⓘ

BBB↑, 1,  

Immune & Inflammatory Signaling ⓘ

IL1β↓, 1,   Inflam↓, 1,  

Protein Aggregation ⓘ

Aβ↓, 1,  

Drug Metabolism & Resistance ⓘ

BioAv↓, 2,   BioAv↑, 2,   Half-Life↓, 1,  

Functional Outcomes ⓘ

cognitive↑, 1,   neuroP↑, 2,  
Total Targets: 29

Scientific Paper Hit Count for: G6PD, Glucose-6-phosphate dehydrogenase
1 Resveratrol
1 Sulforaphane (mainly Broccoli)
1 Vitamin B5,Pantothenic Acid
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#:808  State#:%  Dir#:2
  wNotes=on  sortOrder:rid,rpid

 

Home Page