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.
GBM, Glioblastoma: Click to Expand ⟱
Glioblastoma is a fast-growing and aggressive brain tumor.
Scientific Papers found: Click to Expand⟱
3345- ART/DHA,    Dihydroartemisinin-induced unfolded protein response feedback attenuates ferroptosis via PERK/ATF4/HSPA5 pathway in glioma cells
- in-vitro, GBM, NA
ROS↑, Ferroptosis↑, lipid-P↑, HSP70/HSPA5↑, ER Stress↑, ATF4↑, GRP78/BiP↑, MDA↑, GSH↓, eff↑, GPx4↑,
739- Bor,    Borax regulates iron chaperone- and autophagy-mediated ferroptosis pathway in glioblastoma cells
- in-vitro, GBM, U87MG - in-vitro, Nor, HMC3
TumCG↓, TumCP↓, TumCCA↑, PCBP1↓, GSH↓, GPx4↓, Beclin-1↑, MDA↑, ACSL4↑, Casp3↑, Casp7↑, Ferroptosis↑, *toxicity↓,
738- Bor,    Borax induces ferroptosis of glioblastoma by targeting HSPA5/NRF2/GPx4/GSH pathways
- in-vitro, GBM, U251 - in-vitro, GBM, A172 - in-vitro, Nor, SVGp12
TumCP↓, GPx4↓, GSH↓, HSP70/HSPA5↓, NRF2↓, MDA↑, Casp3↑, Casp7↑, Ferroptosis↑, selectivity↑,
729- Bor,    Promising potential of boron compounds against Glioblastoma: In Vitro antioxidant, anti-inflammatory and anticancer studies
- in-vitro, GBM, U87MG - in-vivo, Nor, HaCaT
TOS↑, TumCG↓, MDA↑, SOD↑, Catalase↑, TAC↓, GSH↓, BRAF↑, MAPK↓, PTEN↓, Raf↓, *toxicity↓,
2273- dietMet,    Methionine and cystine double deprivation stress suppresses glioma proliferation via inducing ROS/autophagy
- in-vitro, GBM, U87MG - in-vitro, GBM, U251 - in-vivo, NA, NA
ROS↑, GSH↓, TumCP↓, TumAuto↑, LC3II↑,
5099- JG,    Juglone induces ferroptosis in glioblastoma cells by inhibiting the Nrf2-GPX4 axis through the phosphorylation of p38MAPK
- vitro+vivo, GBM, LN229 - vitro+vivo, GBM, T98G
Ferroptosis↑, p‑MAPK↑, NRF2↓, GPx4↓, TumPF↓, Apoptosis↑, ROS↑, GSH↓, lipid-P↑, Ki-67↓, TumCG↓,
184- MFrot,  MF,    Rotating Magnetic Fields Inhibit Mitochondrial Respiration, Promote Oxidative Stress and Produce Loss of Mitochondrial Integrity in Cancer Cells
- in-vitro, GBM, GBM
ROS↑, mitResp↓, mtDam↑, Dose↝, MMP?, OCR↓, mt-H2O2↑, eff↓, SDH↓, Thiols↓, GSH↓, TumCD↑, Casp3↑, Casp7↑, MPT↑, Cyt‑c↑, selectivity↑, GSH/GSSG↓, ETC↓,
1940- PL,    Piperlongumine Inhibits Migration of Glioblastoma Cells via Activation of ROS-Dependent p38 and JNK Signaling Pathways
- in-vitro, GBM, LN229 - in-vitro, GBM, U87MG
ROS↑, GSH↓, p38↑, JNK↑, IKKα↑, NF-kB↓, eff↓,
2949- PL,    Piperlongumine selectively kills glioblastoma multiforme cells via reactive oxygen species accumulation dependent JNK and p38 activation
- in-vitro, GBM, LN229 - in-vitro, GBM, U87MG
selectivity↑, ROS↑, JNK↑, p38↑, GSH↓, eff↓,
2951- PL,  AF,    Synergistic Dual Targeting of Thioredoxin and Glutathione Systems Irrespective of p53 in Glioblastoma Stem Cells
- in-vitro, GBM, U87MG
GSH↓, eff↑, GSTP1/GSTπ↓,
5040- SAS,    Structure-Activity-Relationship-Aided Design and Synthesis of xCT Antiporter Inhibitors
- in-vitro, GBM, A172 - in-vitro, Melanoma, A375 - in-vitro, GBM, U87MG - in-vitro, BC, MCF-7
GSH↓, toxicity↓, xCT↓,
5138- SAS,  Rad,    Drug repurposing: sulfasalazine sensitizes gliomas to gamma knife radiosurgery by blocking cystine uptake through system Xc-, leading to glutathione depletion
- vitro+vivo, GBM, NA
cystine↓, GSH↓, ROS↑, RadioS↑, eff↓, DNAdam↑, OS↑,
2410- SIL,    Autophagy activated by silibinin contributes to glioma cell death via induction of oxidative stress-mediated BNIP3-dependent nuclear translocation of AIF
- in-vitro, GBM, U87MG - in-vitro, GBM, U251 - in-vivo, NA, NA
TumAuto↑, ATP↓, Glycolysis↓, H2O2↑, P53↑, GSH↓, xCT↓, BNIP3↝, MMP↑, mt-ROS↑, mtDam↑, HK2↓, PFKP↓, PKM2↓, TumCG↓,
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↑, RIP3↑, Glycolysis↓, G6PD↓, HK2↓, PKM2↓, H2O2↑, GSH↓, ROS↑,
1342- SK,    RIP1 and RIP3 contribute to shikonin-induced DNA double-strand breaks in glioma cells via increase of intracellular reactive oxygen species
- in-vitro, GBM, NA - in-vivo, NA, NA
RIP1↑, RIP3↑, DNAdam↑, ROS↑, GSH↓,
1344- SK,    Novel multiple apoptotic mechanism of shikonin in human glioma cells
- in-vitro, GBM, U87MG - in-vitro, GBM, Hs683 - in-vitro, GBM, M059K
ROS↑, GSH↓, MMP↓, P53↑, cl‑PARP↑, Catalase↓, SOD1↑, Bcl-2↓, BAX↑, eff↓,
1346- SK,    An Oxidative Stress Mechanism of Shikonin in Human Glioma Cells
- in-vitro, GBM, U87MG - in-vitro, GBM, Hs683
NRF2↓, ROS↑, Apoptosis↑, Cyt‑c↑, GSH↓, MMP↓, P53↑, HO-1⇅,
5091- SSE,    Superoxide-mediated ferroptosis in human cancer cells induced by sodium selenite
- in-vitro, GBM, U87MG - in-vitro, Cerv, HeLa - in-vitro, BC, MCF-7 - in-vitro, Pca, PC3 - in-vitro, CRC, HT-29 - in-vitro, Nor, SVGp12
Ferroptosis↑, xCT↓, GSH↓, GPx4↓, Iron↑, lipid-P↑, ROS↑, eff↓, TumCP↓, TumCD↑,
5088- SSE,    Superoxide-mediated ferroptosis in human cancer cells induced by sodium selenite
- in-vitro, BC, MCF-7 - in-vitro, GBM, U87MG - in-vitro, Pca, PC3 - in-vitro, Cerv, HeLa - in-vitro, GBM, A172
Ferroptosis↑, ROS↑, Iron↑, xCT↓, GSH↓, GPx4↓, lipid-P↑, TumCP↓, selectivity↑,

Showing Research Papers: 1 to 19 of 19

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 19

Pathway results for Effect on Cancer / Diseased Cells:


Redox & Oxidative Stress ⓘ

Catalase↓, 1,   Catalase↑, 1,   cystine↓, 1,   Ferroptosis↑, 6,   GPx4↓, 5,   GPx4↑, 1,   GSH↓, 19,   GSH/GSSG↓, 1,   GSTP1/GSTπ↓, 1,   H2O2↑, 2,   mt-H2O2↑, 1,   HO-1⇅, 1,   Iron↑, 2,   lipid-P↑, 4,   MDA↑, 4,   NRF2↓, 3,   ROS↑, 13,   mt-ROS↑, 1,   SOD↑, 1,   SOD1↑, 1,   TAC↓, 1,   Thiols↓, 1,   TOS↑, 1,   xCT↓, 4,  

Mitochondria & Bioenergetics ⓘ

ATP↓, 1,   ETC↓, 1,   mitResp↓, 1,   MMP?, 1,   MMP↓, 2,   MMP↑, 1,   MPT↑, 1,   mtDam↑, 2,   OCR↓, 1,   Raf↓, 1,   SDH↓, 1,  

Core Metabolism/Glycolysis ⓘ

ACSL4↑, 1,   G6PD↓, 1,   Glycolysis↓, 2,   HK2↓, 2,   PFKP↓, 1,   PKM2↓, 2,  

Cell Death ⓘ

Apoptosis↑, 2,   BAX↑, 1,   Bcl-2↓, 1,   Casp3↑, 3,   Casp7↑, 3,   Cyt‑c↑, 2,   Ferroptosis↑, 6,   JNK↑, 2,   MAPK↓, 1,   p‑MAPK↑, 1,   p38↑, 2,   RIP1↑, 2,   TumCD↑, 2,  

Protein Folding & ER Stress ⓘ

ER Stress↑, 1,   GRP78/BiP↑, 1,   HSP70/HSPA5↓, 1,   HSP70/HSPA5↑, 1,  

Autophagy & Lysosomes ⓘ

Beclin-1↑, 1,   BNIP3↝, 1,   LC3II↑, 1,   TumAuto↑, 2,  

DNA Damage & Repair ⓘ

DNAdam↑, 2,   P53↑, 3,   cl‑PARP↑, 1,  

Cell Cycle & Senescence ⓘ

TumCCA↑, 1,  

Proliferation, Differentiation & Cell State ⓘ

BRAF↑, 1,   PTEN↓, 1,   TumCG↓, 4,  

Migration ⓘ

Ki-67↓, 1,   PCBP1↓, 1,   RIP3↑, 2,   TumCP↓, 5,   TumPF↓, 1,  

Angiogenesis & Vasculature ⓘ

ATF4↑, 1,  

Immune & Inflammatory Signaling ⓘ

IKKα↑, 1,   NF-kB↓, 1,  

Drug Metabolism & Resistance ⓘ

Dose↝, 1,   eff↓, 6,   eff↑, 2,   RadioS↑, 1,   selectivity↑, 4,  

Clinical Biomarkers ⓘ

BRAF↑, 1,   Ki-67↓, 1,  

Functional Outcomes ⓘ

OS↑, 1,   toxicity↓, 1,  
Total Targets: 86

Pathway results for Effect on Normal Cells:


Functional Outcomes ⓘ

toxicity↓, 2,  
Total Targets: 1

Scientific Paper Hit Count for: GSH, Glutathione
4 Shikonin
3 Boron
3 Piperlongumine
2 Sulfasalazine
2 Selenite (Sodium)
1 Artemisinin
1 diet Methionine-Restricted Diet
1 Juglone
1 Magnetic Field Rotating
1 Magnetic Fields
1 Auranofin
1 Radiotherapy/Radiation
1 Silymarin (Milk Thistle) silibinin
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:27  Cells:%  prod#:%  Target#:137  State#:%  Dir#:1
  wNotes=0  sortOrder:rid,rpid

 

Home Page