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⟱
1274- Cin,    Cinnamon bark extract suppresses metastatic dissemination of cancer cells through inhibition of glycolytic metabolism
- vitro+vivo, BC, MDA-MB-231
TumCI↓, CBE decreased cell motility and invasion of MDA-MB-231 human breast cancer cells without affecting their cell viability
G6PD↓,
HK2↓,
Glycolysis↓, CBE suppresses metastatic dissemination of cancer cells through inhibition of glycolysis metabolism.

3276- Lyco,    Lycopene modulates cellular proliferation, glycolysis and hepatic ultrastructure during hepatocellular carcinoma
- in-vivo, HCC, NA
G6PD↓, Moreover, NDEA treatment caused a significant increase in liver G6PD activity in the NDEA group when compared to the control and LycT groups.
PCNA↓, The LycT + NDEA group showed a significant decrease in mRNA expression of PCNA and Cyclin D1 when compared to the NDEA group
cycD1/CCND1↓,
P21↑, A significant increase in the expression of p21 was observed in the LycT + NDEA group when compared to the contro
Hif1a↓, Pre-treatment with LycT in NDEA-challenged mice resulted in a significant reduction in the expression of HIF-1α at week 24 when compared to the NDEA group
Glycolysis↓, Moreover, significant reductions in the activities of glycolytic enzymes following LycT pre-treatment in NDEA-challenged mice were inversely related to HCC development.

2332- RES,    Resveratrol’s Anti-Cancer Effects through the Modulation of Tumor Glucose Metabolism
- Review, Var, NA
Glycolysis↓, Resveratrol reduces glucose uptake and glycolysis by affecting Glut1, PFK1, HIF-1α, ROS, PDH, and the CamKKB/AMPK pathway.
GLUT1↓, resveratrol reduces glycolytic flux and Glut1 expression by targeting ROS-mediated HIF-1α activation in Lewis lung carcinoma tumor-bearing mice
PFK1↓,
Hif1a↓, Resveratrol specifically suppresses the nuclear β-catenin protein by inhibiting HIF-1α
ROS↑, Resveratrol increases ROS production
PDH↑, leading to increased PDH activity, inhibiting HK and PFK, and downregulating PKM2 activity
AMPK↑, esveratrol elevated NAD+/NADH, subsequently activated Sirt1, and in turn activated the AMP-activated kinase (AMPK),
TumCG↓, inhibits cell growth, invasion, and proliferation by targeting NF-kB, Sirt1, Sirt3, LDH, PI-3K, mTOR, PKM2, R5P, G6PD, TKT, talin, and PGAM.
TumCI↓,
TumCP↓,
p‑NF-kB↓, suppressing NF-κB phosphorylation
SIRT1↑, Resveratrol activates the target subcellular histone deacetylase Sirt1 in various human tissues, including tumors
SIRT3↑,
LDH↓, decreases glycolytic enzymes (pyruvate kinase and LDH) in Caco2 and HCT-116 cells
PI3K↓, Resveratrol also targets “classical” tumor-promoting pathways, such as PI3K/Akt, STAT3/5, and MAPK, which support glycolysis
mTOR↓, AMPK activation further inhibits the mTOR pathway
PKM2↓, inhibiting HK and PFK, and downregulating PKM2 activity
R5P↝,
G6PD↓, G6PDH knockdown significantly reduced cell proliferation
TKT↝,
talin↓, induces apoptosis by targeting the pentose phosphate and talin-FAK signaling pathways
HK2↓, Resveratrol downregulates glucose metabolism, mainly by inhibiting HK2;
GRP78/BiP↑, resveratrol stimulates GRP-78, and decreases glucose uptake,
GlucoseCon↓,
ER Stress↑, resveratrol-induced ER-stress leads to apoptosis of CRC cells
Warburg↓, Resveratrol reverses the Warburg effect
PFK↓, leading to increased PDH activity, inhibiting HK and PFK, and downregulating PKM2 activity

2362- SK,    RIP1 and RIP3 contribute to shikonin-induced glycolysis suppression in glioma cells via increase of intracellular hydrogen peroxide
- in-vitro, GBM, U87MG - in-vivo, GBM, NA - in-vitro, GBM, U251
RIP1↑, we found shikonin activated RIP1 and RIP3 in glioma cells in vitro and in vivo, which was accompanied with glycolysis suppression
RIP3↑,
Glycolysis↓,
G6PD↓, shikonin-induced decreases of glucose-6-phosphate and pyruvate and downregulation of HK II and PKM2
HK2↓,
PKM2↓,
H2O2↑, shikonin also triggered accumulation of intracellular H2O2 and depletion of GSH and cysteine
GSH↓,
ROS↑, It was documented that inhibition of HK II with its inhibitor 3-bromopyruvate or knockdown of its level resulted in accumulation of ROS


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 ⓘ

GSH↓, 1,   H2O2↑, 1,   ROS↑, 2,   SIRT3↑, 1,   TKT↝, 1,  

Core Metabolism/Glycolysis ⓘ

AMPK↑, 1,   G6PD↓, 4,   GlucoseCon↓, 1,   Glycolysis↓, 4,   HK2↓, 3,   LDH↓, 1,   PDH↑, 1,   PFK↓, 1,   PFK1↓, 1,   PKM2↓, 2,   R5P↝, 1,   SIRT1↑, 1,   Warburg↓, 1,  

Cell Death ⓘ

RIP1↑, 1,  

Protein Folding & ER Stress ⓘ

ER Stress↑, 1,   GRP78/BiP↑, 1,  

DNA Damage & Repair ⓘ

PCNA↓, 1,  

Cell Cycle & Senescence ⓘ

cycD1/CCND1↓, 1,   P21↑, 1,  

Proliferation, Differentiation & Cell State ⓘ

mTOR↓, 1,   PI3K↓, 1,   TumCG↓, 1,  

Migration ⓘ

RIP3↑, 1,   talin↓, 1,   TumCI↓, 2,   TumCP↓, 1,  

Angiogenesis & Vasculature ⓘ

Hif1a↓, 2,  

Barriers & Transport ⓘ

GLUT1↓, 1,  

Immune & Inflammatory Signaling ⓘ

p‑NF-kB↓, 1,  

Clinical Biomarkers ⓘ

LDH↓, 1,  
Total Targets: 35

Pathway results for Effect on Normal Cells:


Total Targets: 0

Scientific Paper Hit Count for: G6PD, Glucose-6-phosphate dehydrogenase
1 Cinnamon
1 Lycopene
1 Resveratrol
1 Shikonin
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#:1
  wNotes=on  sortOrder:rid,rpid

 

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