GSTs Cancer Research Results

GSTs, Glutathione S-transferases: Click to Expand ⟱
Source:
Type:
Glutathione S-transferases (GSTs) are a family of phase II detoxification enzymes that play key roles in catalyzing the conjugation of glutathione (GSH) to a wide range of electrophilic compounds. This family includes multiple isoenzymes (e.g., GST-α, GST-μ, GST-π) with tissue-specific expression patterns and overlapping as well as distinct substrate specificities.

-GSTs are important for detoxifying potentially harmful compounds, including products of oxidative stress, environmental toxins, and chemotherapeutic agents.
-They contribute to the cellular defense mechanism against oxidative damage and help maintain cellular redox balance.
-Beyond detoxification, GSTs can modulate cell signaling pathways, potentially affecting cell proliferation, apoptosis, and drug resistance.

-GST-π is commonly upregulated in several cancers such as breast, lung, colorectal, and hematologic malignancies.
-Elevated expression of specific GST isoenzymes—most notably GST-π—has been associated with a poorer prognosis in several cancer types. This is often linked to resistance to chemo- or radiotherapy, as higher GST activity can lead to more efficient detoxification of these agents, reducing their cytotoxic effects.
-In contrast, reduced GST expression in some contexts might indicate a less robust detoxification system, which can correlate with increased sensitivity to oxidative stress and possibly a less aggressive tumor phenotype.
Liver, Liver Cancer: Click to Expand ⟱
Liver Cancer
Scientific Papers found: Click to Expand⟱
2859- FIS,    The Natural Flavonoid Fisetin Inhibits Cellular Proliferation of Hepatic, Colorectal, and Pancreatic Cancer Cells through Modulation of Multiple Signaling Pathways
- in-vitro, Liver, HepG2 - NA, Colon, Caco-2
TumCG↓, other↝, Casp3↑, Casp7↑, PGE2↓, GSTs↓, Wnt↓, EGFR↓, NF-kB↓, COX2↓, P53↑, P21↑, P450↓,
2922- LT,    Combination of transcriptomic and proteomic approaches helps unravel the mechanisms of luteolin in inducing liver cancer cell death via targeting AKT1 and SRC
- in-vitro, Liver, HUH7
Half-Life↝, TumCCA↑, AKT1↓, ATF2↓, NF-kB↓, GSK‐3β↓, cMyc↓, GSTs↓, TrxR1↓, ROS↑,

Showing Research Papers: 1 to 2 of 2

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 2

Pathway results for Effect on Cancer / Diseased Cells:


Redox & Oxidative Stress ⓘ

GSTs↓, 2,   ROS↑, 1,   TrxR1↓, 1,  

Core Metabolism/Glycolysis ⓘ

AKT1↓, 1,   cMyc↓, 1,  

Cell Death ⓘ

ATF2↓, 1,   Casp3↑, 1,   Casp7↑, 1,  

Transcription & Epigenetics ⓘ

other↝, 1,  

DNA Damage & Repair ⓘ

P53↑, 1,  

Cell Cycle & Senescence ⓘ

P21↑, 1,   TumCCA↑, 1,  

Proliferation, Differentiation & Cell State ⓘ

GSK‐3β↓, 1,   TumCG↓, 1,   Wnt↓, 1,  

Angiogenesis & Vasculature ⓘ

EGFR↓, 1,  

Immune & Inflammatory Signaling ⓘ

COX2↓, 1,   NF-kB↓, 2,   PGE2↓, 1,  

Drug Metabolism & Resistance ⓘ

Half-Life↝, 1,   P450↓, 1,  

Clinical Biomarkers ⓘ

EGFR↓, 1,  
Total Targets: 22

Pathway results for Effect on Normal Cells:


Total Targets: 0

Scientific Paper Hit Count for: GSTs, Glutathione S-transferases
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:14  Cells:%  prod#:%  Target#:1153  State#:%  Dir#:1
  wNotes=0  sortOrder:rid,rpid

 

Home Page