erastin / GSH Cancer Research Results

erastin, erastin: Click to Expand ⟱
Features:
Erastin is often referred to as a "metabolic inhibitor" or a "ferroptosis inducer", rather than a traditional chemotherapy agent.
Erastin is primarily available as a research chemical—it's not an approved therapeutic for clinical use.

Pathways:
-Erastin inhibits system xCT, thereby reducing cystine uptake. This leads to decreased intracellular cysteine, a precursor for GSH. As a consequence, the cell’s glutathione levels drop, compromising its ability to neutralize reactive oxygen species (ROS).
-Glutathione (GSH) Depletion and Increased Oxidative Stress
-Voltage-Dependent Anion Channels (VDACs): Altering VDAC function can affect mitochondrial metabolism, leading to changes in energy production and further enhancing oxidative stress.


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.


Scientific Papers found: Click to Expand⟱
727- Bor,  RSL3,  erastin,    Enhancement of ferroptosis by boric acid and its potential use as chemosensitizer in anticancer chemotherapy
- in-vitro, Liver, HepG2
ROS↑, GSH↓, TBARS↑, Ferroptosis↑, ChemoSen↑,
2204- erastin,    Regulation of ferroptotic cancer cell death by GPX4
- in-vitro, fibroS, HT1080
GSH↓, Ferroptosis↑, ROS↑, GPx↓, GPx4↓, lipid-P↑, eff↓, eff↑,
2455- erastin,    Discovery of the Inhibitor Targeting the SLC7A11/xCT Axis through In Silico and In Vitro Experiments
- in-vitro, Cerv, HeLa
xCT↓, GSH↓, ROS↑, TumCMig↓,
5046- erastin,  SAS,    The structure of erastin-bound xCT–4F2hc complex reveals molecular mechanisms underlying erastin-induced ferroptosis
- Study, Var, NA
xCT↓, ROS↑, TumCG↓, GSH↓, Ferroptosis↑,
5047- erastin,    The ferroptosis inducer erastin irreversibly inhibits system xc− and synergizes with cisplatin to increase cisplatin’s cytotoxicity in cancer cells
- in-vitro, Ovarian, NA
xCT↓, GSH↓, Ferroptosis↑, ChemoSen↑, eff↑,

Showing Research Papers: 1 to 5 of 5

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 5

Pathway results for Effect on Cancer / Diseased Cells:


Redox & Oxidative Stress

Ferroptosis↑, 4,   GPx↓, 1,   GPx4↓, 1,   GSH↓, 5,   lipid-P↑, 1,   ROS↑, 4,   TBARS↑, 1,   xCT↓, 3,  

Cell Death

Ferroptosis↑, 4,  

Proliferation, Differentiation & Cell State

TumCG↓, 1,  

Migration

TumCMig↓, 1,  

Drug Metabolism & Resistance

ChemoSen↑, 2,   eff↓, 1,   eff↑, 2,  
Total Targets: 14

Pathway results for Effect on Normal Cells:


Total Targets: 0

Scientific Paper Hit Count for: GSH, Glutathione
5 erastin
1 Boron
1 Ras-selective lethal 3
1 Sulfasalazine
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#:241  Target#:137  State#:%  Dir#:1
wNotes=0 sortOrder:rid,rpid

 

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