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.
TumMeta↓,

6161- Cin,    Cinnamon bark extract suppresses metastatic dissemination of cancer cells through inhibition of glycolytic metabolism
- in-vivo, BC, MDA-MB-231
TumMeta↓, Here we report that cinnamon bark extract (CBE) has a suppressor effect on metastatic dissemination of cancer cells
HK2↓, CBE decreased the expression of hexokinase 2 (HK2), which catalyzes G6P production, and pharmacological inhibition of HK2 suppressed cell invasion and migration of MDA-MB-231 cells
TumCI↓,
TumCMig↓,
Glycolysis↓, CBE suppressed metastatic dissemination of human cancer cells by inhibiting glycolytic metabolism.
G6PD↓, We demonstrated that CBE decreased HK2 expression and that disrupted the production of G6P and F6P, which are intermediate metabolites of glycolytic metabolism.

6223- CUR,    Curcumin Rewires the Tumor Metabolic Landscape: Mechanisms and Clinical Prospects
- Review, Var, NA
Ferroptosis↑, including the induction of ferroptosis by regulating the SLC7A11/GPX4 axis
GutMicro↑, and modulating gut microbiota metabolism. I
Akt↓, it inhibits pro-tumorigenic signals such as Akt/mTOR, NF-κB, Wnt/β-catenin, and STAT3, thereby blocking tumor proliferation, invasion, and metastasis
mTOR↓,
NF-kB↓,
Wnt↓,
β-catenin/ZEB1↓,
STAT3↓,
TumCP↓,
TumCI↓,
TumMeta↓,
AMPK↑, activates tumor-suppressive and cytoprotective pathways, including AMPK, p53, and nuclear factor erythroid 2-related factor 2 (Nrf2), which induce cell cycle arrest and apoptosis
P53↑,
NRF2↑,
TumCCA↑,
Apoptosis↑,
Casp↑, activation of the Caspase cascade
GPx4↓, as well as ferroptosis by inhibiting the solute carrier family 7 member 11 (SLC7A11)/glutathione peroxidase 4 (GPX4) axis [5]
DNMTs↓, inhibiting epigenetic regulatory mechanisms such as DNMTs and HDACs.
HDAC↓,
VEGF↓, inhibiting VEGF signaling and enhances the immune microenvironment by improving T cell and NK cell function
Imm↑,
NK cell↑,
Warburg↓, Curcumin effectively reverses the Warburg effect and interferes with glucose metabolism by targeting HIF-1α and inhibiting key enzymes, including hexokinase 2 (HK2), pyruvate kinase M2 (PKM2), and lactate dehydrogenase A (LDHA)
Hif1a↓,
HK2↓,
PKM2↓,
LDHA↓,
GLUT1↓, as well as the functions of glucose transporter 1 (GLUT1) and monocarboxylate transporters (MCTs) [12].
MCT1↓,
AMPK↑, curcumin activates signaling pathways such as AMPK, downregulates fatty acid synthase (FASN) and stearoyl-CoA desaturase (SCD1),
FASN↓,
SCD1↓,
GLS↓, Curcumin extensively intervenes in amino acid metabolism by inhibiting the activity of glutaminase (GLS), ornithine decarboxylase (ODC), and other enzymes,
Apoptosis↑, inducing apoptosis through mechanisms such as disrupting the electron transport chain, reducing membrane potential, and promoting the generation of reactive oxygen species (ROS)
ETC↓,
MMP↓,
ROS↑,
lipid-P↑, curcumin induces lipid peroxidation and collapses redox homeostasis, thereby activating the ferroptosis program [
ChemoSen↑, blocking invasion and metastasis, and enhancing chemosensitivity.
PDK1↓, In hypoxic pancreatic cancer cells, curcumin downregulates the expression of GLUT1, HK2, LDHA, and PDK1 by inhibiting the Beclin1/HIF-1α axis, which results in reduced ATP production and inhibited cell proliferation [
Beclin-1↓,
ATP↓,
Glycolysis↓, inhibiting glycolysis
GlucoseCon↓, decreased glucose uptake and increased lactate production
lactateProd↑,
MMPs↓, reduces MMP, GSH, and G6PD activities
GSH↓, inhibition of SLC7A11 to limit GSH synthesis, thereby triggering the collapse of the antioxidant defense system
G6PD↓,
OXPHOS↓, downregulate OXPHOS and glycolysis activities
SREBP2↓, curcumin treatment leads to a marked downregulation of the mRNA expression of SREBP and its target genes. inhibiting the expression of NPC1L1, SREBP-2, and HNF1α
COX2↓, curcumin exerts anti-tumor effects by downregulating the expression of NF-κB, COX-2, and AP-1
AP-1↓,
NADH↓, decreased GPx4 and FSP1 expression, induced ferroptosis by inhibiting GSH-GPx4 and FSP1-CoQ 10-NADH pathways
NRF2↑, it inhibits GPX4 and activates Nrf2 and heme oxygenase-1 (HO-1). This results in an abnormal accumulation of intracellular Fe2+, ROS, lipid peroxides, and malondialdehyde (MDA), along with a depletion of GSH
HO-1↑,
Iron↑,
MDA↑,
*ROS↓, studies have demonstrated that the topical application of curcumin on the skin exerts antitumor effects by synergistically downregulating COX-2 and ODC activities, alleviating oxidative damage, and concurrently inhibiting inflammatory proliferation i
*Inflam↓,

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 6 of 6

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 6

Pathway results for Effect on Cancer / Diseased Cells:


Redox & Oxidative Stress ⓘ

Ferroptosis↑, 1,   GPx4↓, 1,   GSH↓, 2,   H2O2↑, 1,   HO-1↑, 1,   Iron↑, 1,   lipid-P↑, 1,   MDA↑, 1,   NADH↓, 1,   NRF2↑, 2,   OXPHOS↓, 1,   ROS↑, 3,   SIRT3↑, 1,   TKT↝, 1,  

Mitochondria & Bioenergetics ⓘ

ATP↓, 1,   ETC↓, 1,   MMP↓, 1,  

Core Metabolism/Glycolysis ⓘ

AMPK↑, 3,   FASN↓, 1,   G6PD↓, 6,   GLS↓, 1,   GlucoseCon↓, 2,   Glycolysis↓, 6,   HK2↓, 5,   lactateProd↑, 1,   LDH↓, 1,   LDHA↓, 1,   PDH↑, 1,   PDK1↓, 1,   PFK↓, 1,   PFK1↓, 1,   PKM2↓, 3,   R5P↝, 1,   SCD1↓, 1,   SIRT1↑, 1,   SREBP2↓, 1,   Warburg↓, 2,  

Cell Death ⓘ

Akt↓, 1,   Apoptosis↑, 2,   Casp↑, 1,   Ferroptosis↑, 1,   MCT1↓, 1,   RIP1↑, 1,  

Protein Folding & ER Stress ⓘ

ER Stress↑, 1,   GRP78/BiP↑, 1,  

Autophagy & Lysosomes ⓘ

Beclin-1↓, 1,  

DNA Damage & Repair ⓘ

DNMTs↓, 1,   P53↑, 1,   PCNA↓, 1,  

Cell Cycle & Senescence ⓘ

cycD1/CCND1↓, 1,   P21↑, 1,   TumCCA↑, 1,  

Proliferation, Differentiation & Cell State ⓘ

HDAC↓, 1,   mTOR↓, 2,   PI3K↓, 1,   STAT3↓, 1,   TumCG↓, 1,   Wnt↓, 1,  

Migration ⓘ

AP-1↓, 1,   MMPs↓, 1,   RIP3↑, 1,   talin↓, 1,   TumCI↓, 4,   TumCMig↓, 1,   TumCP↓, 2,   TumMeta↓, 3,   β-catenin/ZEB1↓, 1,  

Angiogenesis & Vasculature ⓘ

Hif1a↓, 3,   VEGF↓, 1,  

Barriers & Transport ⓘ

GLUT1↓, 2,  

Immune & Inflammatory Signaling ⓘ

COX2↓, 1,   Imm↑, 1,   NF-kB↓, 1,   p‑NF-kB↓, 1,   NK cell↑, 1,  

Drug Metabolism & Resistance ⓘ

ChemoSen↑, 1,  

Clinical Biomarkers ⓘ

GutMicro↑, 1,   LDH↓, 1,  
Total Targets: 78

Pathway results for Effect on Normal Cells:


Redox & Oxidative Stress ⓘ

ROS↓, 1,  

Immune & Inflammatory Signaling ⓘ

Inflam↓, 1,  
Total Targets: 2

Scientific Paper Hit Count for: G6PD, Glucose-6-phosphate dehydrogenase
2 Cinnamon
1 Curcumin
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

 

Home Page