GSH Cancer Research Results

GSH, Glutathione: Click to Expand ⟱
Source:
Type:
Glutathione (GSH) is a thiol antioxidant that scavenges reactive oxygen species (ROS), resulting in the formation of oxidized glutathione (GSSG). Decreased amounts of GSH and a decreased GSH/GSSG ratio in tissues are biomarkers of oxidative stress.
Glutathione is a powerful antioxidant found in every cell of the body, composed of three amino acids: cysteine, glutamine, and glycine. It plays a crucial role in protecting cells from oxidative stress, detoxifying harmful substances, and supporting the immune system.
cancer cells can have elevated levels of glutathione, which may help them survive in the oxidative environment created by the immune response and chemotherapy. This can make cancer cells more resistant to treatment.
While glutathione can be obtained from certain foods (like fruits, vegetables, and meats), its absorption from supplements is debated. Some people take N-acetylcysteine (NAC) or other precursors to boost glutathione levels, but the effects on cancer prevention or treatment are still being studied.
Depleting glutathione (GSH) to raise reactive oxygen species (ROS) is a strategy that has been explored in cancer research and therapy.
Many cancer cells have altered redox states and may rely on GSH to survive. Increasing ROS levels can induce stress in these cells, potentially leading to cell death.
Certain drugs and compounds can deplete GSH levels. For example, agents like buthionine sulfoximine (BSO) inhibit the synthesis of GSH, leading to its depletion.
Cancer cells tend to exhibit higher levels of intracellular GSH, possibly as an adaptive response to a higher metabolism and thus higher steady-state levels of reactive oxygen species (ROS).

"...intracellular glutathione (GSH) exhibits an astounding antioxidant activity in scavenging reactive oxygen species (ROS)..."
"Cancer cells have a high level of GSH compared to normal cells."
"...cancer cells are affluent with high antioxidant levels, especially with GSH, whose appearance at an elevated concentration of ∼10 mM (10 times less in normal cells) detoxifies the cancer cells." "Therefore, GSH depletion can be assumed to be the key strategy to amplify the oxidative stress in cancer cells, enhancing the destruction of cancer cells by fruitful cancer therapy."

The loss of GSH is broadly known to be directly related to the apoptosis progression.
Pca, Prostate Cancer: Click to Expand ⟱
Prostate Cancer: Alterations in genes such as ERG, SPOP, MYC, androgen receptor (AR), and CHD1, drive PCa progression.
TP53 is the most commonly mutated gene in human cancer.
HH↑, GLI-1↑, SHH↑ P53↓
The loss of p53 and/or other tumor suppressor genes, reduced capacity for DNA repair, the dysfunction of telomerase activity, and changes in the pathways that govern the growth of cells also mediate the progression of Pca.
It has been well documented that Ca2+ influx and MDR1 upregulation are highly associated with GEM metabolism in human pancreatic carcinoma.
Increased Growth factor IGF-1/IGF-1R axis activation mediated by both PI3K/Akt or RAF/MEK/ERK system and AR expression remains important in the development and progression of prostate cancer.
It has been demonstrated that prostate cancer cells are relatively sensitive to heat stress.
Long non-coding RNA MALAT1 has been reported as an oncogenic target in multiple types of cancers, including PC.
Scientific Papers found: Click to Expand⟱
128- CUR,  RES,    Evaluation of biophysical as well as biochemical potential of curcumin and resveratrol during prostate cancer
- in-vivo, Pca, NA
lipid-P↓, chemoPv↑, GSH↑, SOD↑, GSTs↑, glucose↓,
1987- PTL,  Rad,    A NADPH oxidase dependent redox signaling pathway mediates the selective radiosensitization effect of parthenolide in prostate cancer cells
- in-vitro, Pca, PC3 - in-vitro, Nor, PrEC
selectivity↑, RadioS↑, ROS↑, *ROS∅, NADPH↑, Trx↓, PI3K↑, Akt↑, p‑FOXO3↓, SOD2↓, Catalase↓, radioP↑, *NADPH∅, *GSH↑, *GSH/GSSG↑, *NRF2↑,
79- QC,    Chemopreventive Effect of Quercetin in MNU and Testosterone Induced Prostate Cancer of Sprague-Dawley Rats
- in-vivo, Pca, NA
GSH↑, SOD↑, Catalase↑, GPx↑, GSR↑, IGF-1R↓, Akt↓, AR↓, TumCP↓, lipid-P↓, H2O2↓, Raf↓, p‑MEK↓, Bcl-2↑, Bcl-xL↑, Casp3↑, Casp8↑, Casp9↑,
3369- QC,    Pharmacological basis and new insights of quercetin action in respect to its anti-cancer effects
- Review, Pca, NA
FAK↓, TumCCA↑, p‑pRB↓, CDK2↑, CycB/CCNB1↓, CDK1↓, EMT↓, PI3K↓, MAPK↓, Wnt↓, ROS↑, miR-21↑, Akt↓, NF-kB↓, FasL↑, Bak↑, BAX↑, Bcl-2↓, Casp3↓, Casp9↑, P53↑, p38↑, MAPK↑, Cyt‑c↑, PARP↓, CHOP↑, ROS↓, LDH↑, GRP78/BiP↑, ERK↑, MDA↓, SOD↑, GSH↑, NRF2↑, VEGF↓, PDGF↓, EGF↓, FGF↓, TNF-α↓, TGF-β↓, VEGFR2↓, EGFR↓, FGFR1↓, mTOR↓, cMyc↓, MMPs↓, LC3B-II↑, Beclin-1↑, IL1β↓, CRP↓, IL10↓, COX2↓, IL6↓, TLR4↓, Shh↓, HER2/EBBR2↓, NOTCH↓, DR5↑, HSP70/HSPA5↓, CSCs↓, angioG↓, MMP2↓, MMP9↓, IGFBP3↑, uPA↓, uPAR↓, RAS↓, Raf↓, TSP-1↑,

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 ⓘ

Catalase↓, 1,   Catalase↑, 1,   GPx↑, 1,   GSH↑, 3,   GSR↑, 1,   GSTs↑, 1,   H2O2↓, 1,   lipid-P↓, 2,   MDA↓, 1,   NRF2↑, 1,   ROS↓, 1,   ROS↑, 2,   SOD↑, 3,   SOD2↓, 1,   Trx↓, 1,  

Mitochondria & Bioenergetics ⓘ

EGF↓, 1,   FGFR1↓, 1,   p‑MEK↓, 1,   Raf↓, 2,  

Core Metabolism/Glycolysis ⓘ

cMyc↓, 1,   glucose↓, 1,   LDH↑, 1,   NADPH↑, 1,  

Cell Death ⓘ

Akt↓, 2,   Akt↑, 1,   Bak↑, 1,   BAX↑, 1,   Bcl-2↓, 1,   Bcl-2↑, 1,   Bcl-xL↑, 1,   Casp3↓, 1,   Casp3↑, 1,   Casp8↑, 1,   Casp9↑, 2,   Cyt‑c↑, 1,   DR5↑, 1,   FasL↑, 1,   MAPK↓, 1,   MAPK↑, 1,   p38↑, 1,  

Kinase & Signal Transduction ⓘ

HER2/EBBR2↓, 1,  

Transcription & Epigenetics ⓘ

miR-21↑, 1,   p‑pRB↓, 1,  

Protein Folding & ER Stress ⓘ

CHOP↑, 1,   GRP78/BiP↑, 1,   HSP70/HSPA5↓, 1,  

Autophagy & Lysosomes ⓘ

Beclin-1↑, 1,   LC3B-II↑, 1,  

DNA Damage & Repair ⓘ

P53↑, 1,   PARP↓, 1,  

Cell Cycle & Senescence ⓘ

CDK1↓, 1,   CDK2↑, 1,   CycB/CCNB1↓, 1,   TumCCA↑, 1,  

Proliferation, Differentiation & Cell State ⓘ

CSCs↓, 1,   EMT↓, 1,   ERK↑, 1,   FGF↓, 1,   p‑FOXO3↓, 1,   IGF-1R↓, 1,   IGFBP3↑, 1,   mTOR↓, 1,   NOTCH↓, 1,   PI3K↓, 1,   PI3K↑, 1,   RAS↓, 1,   Shh↓, 1,   Wnt↓, 1,  

Migration ⓘ

FAK↓, 1,   MMP2↓, 1,   MMP9↓, 1,   MMPs↓, 1,   PDGF↓, 1,   TGF-β↓, 1,   TSP-1↑, 1,   TumCP↓, 1,   uPA↓, 1,   uPAR↓, 1,  

Angiogenesis & Vasculature ⓘ

angioG↓, 1,   EGFR↓, 1,   VEGF↓, 1,   VEGFR2↓, 1,  

Immune & Inflammatory Signaling ⓘ

COX2↓, 1,   CRP↓, 1,   IL10↓, 1,   IL1β↓, 1,   IL6↓, 1,   NF-kB↓, 1,   TLR4↓, 1,   TNF-α↓, 1,  

Hormonal & Nuclear Receptors ⓘ

AR↓, 1,  

Drug Metabolism & Resistance ⓘ

RadioS↑, 1,   selectivity↑, 1,  

Clinical Biomarkers ⓘ

AR↓, 1,   CRP↓, 1,   EGFR↓, 1,   HER2/EBBR2↓, 1,   IL6↓, 1,   LDH↑, 1,  

Functional Outcomes ⓘ

chemoPv↑, 1,   radioP↑, 1,  
Total Targets: 101

Pathway results for Effect on Normal Cells:


Redox & Oxidative Stress ⓘ

GSH↑, 1,   GSH/GSSG↑, 1,   NRF2↑, 1,   ROS∅, 1,  

Core Metabolism/Glycolysis ⓘ

NADPH∅, 1,  
Total Targets: 5

Scientific Paper Hit Count for: GSH, Glutathione
2 Quercetin
1 Curcumin
1 Resveratrol
1 Parthenolide
1 Radiotherapy/Radiation
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:22  Cells:%  prod#:%  Target#:137  State#:%  Dir#:2
  wNotes=0  sortOrder:rid,rpid

 

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