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.
GC, Gastric Adenocarcinoma: Click to Expand ⟱
Stomach/Gastric Cancer
Scientific Papers found: Click to Expand⟱
5501- Ba,    Therapeutic effects and mechanisms of action of Baicalein on stomach cancer: a comprehensive systematic literature review
- Review, GC, NA
AntiCan↑, Apoptosis↑, TumCP↓, TumMeta↓, BAX↑, TumAuto↑, ROS↑, NRF2↝, PI3K↓, Akt↓, NF-kB↓, TGF-β↓, SMAD4↓, GPx4↓, MMP↓, *HO-1↑, *GSTs↑, *antiOx↑, *AntiTum↑, *NRF2↑, ChemoSen↑, Akt↓, mTOR↓, FAK↓, Ki-67↓,
4794- Lyco,    Anticancer Effect of Lycopene in Gastric Carcinogenesis
- Review, GC, NA
*AntiCan↑, *ROS↓, *GSH↑, *GPx↑, *GSTs↑, TumCG↓, Apoptosis↑, ERK↓, Bcl-2↓, BAX↑, Cyt‑c↑, TumCCA↑, *DNAdam↓,

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 ⓘ

GPx4↓, 1,   NRF2↝, 1,   ROS↑, 1,  

Mitochondria & Bioenergetics ⓘ

MMP↓, 1,  

Cell Death ⓘ

Akt↓, 2,   Apoptosis↑, 2,   BAX↑, 2,   Bcl-2↓, 1,   Cyt‑c↑, 1,  

Autophagy & Lysosomes ⓘ

TumAuto↑, 1,  

Cell Cycle & Senescence ⓘ

TumCCA↑, 1,  

Proliferation, Differentiation & Cell State ⓘ

ERK↓, 1,   mTOR↓, 1,   PI3K↓, 1,   TumCG↓, 1,  

Migration ⓘ

FAK↓, 1,   Ki-67↓, 1,   SMAD4↓, 1,   TGF-β↓, 1,   TumCP↓, 1,   TumMeta↓, 1,  

Immune & Inflammatory Signaling ⓘ

NF-kB↓, 1,  

Drug Metabolism & Resistance ⓘ

ChemoSen↑, 1,  

Clinical Biomarkers ⓘ

Ki-67↓, 1,  

Functional Outcomes ⓘ

AntiCan↑, 1,  
Total Targets: 25

Pathway results for Effect on Normal Cells:


Redox & Oxidative Stress ⓘ

antiOx↑, 1,   GPx↑, 1,   GSH↑, 1,   GSTs↑, 2,   HO-1↑, 1,   NRF2↑, 1,   ROS↓, 1,  

DNA Damage & Repair ⓘ

DNAdam↓, 1,  

Functional Outcomes ⓘ

AntiCan↑, 1,   AntiTum↑, 1,  
Total Targets: 10

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:28  Cells:%  prod#:%  Target#:1153  State#:%  Dir#:2
  wNotes=0  sortOrder:rid,rpid

 

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