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.
Melanoma, Melanoma Skin Cancer: Click to Expand ⟱
Melanoma is a rare form of skin cancer. It is more likely to invade nearby tissues and spread to other parts of the body than other types of skin cancer.
Scientific Papers found: Click to Expand⟱
2717- BetA,    Betulinic Acid Induces ROS-Dependent Apoptosis and S-Phase Arrest by Inhibiting the NF-κB Pathway in Human Multiple Myeloma
- in-vitro, Melanoma, U266 - in-vivo, Melanoma, NA - in-vitro, Melanoma, RPMI-8226
Apoptosis↑, TumCCA↑, MMP↓, ROS↑, eff↓, NF-kB↓, Cyt‑c↑, Casp3↑, Casp8↑, Casp9↑, cl‑PARP1↑, MDA↑, SOD↓, SOD2↓, GCLM↓, GSTA1↓, FTH1↓, GSTs↓, TumVol↓,

Showing Research Papers: 1 to 1 of 1

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 1

Pathway results for Effect on Cancer / Diseased Cells:


Redox & Oxidative Stress ⓘ

GCLM↓, 1,   GSTA1↓, 1,   GSTs↓, 1,   MDA↑, 1,   ROS↑, 1,   SOD↓, 1,   SOD2↓, 1,  

Metal & Cofactor Biology ⓘ

FTH1↓, 1,  

Mitochondria & Bioenergetics ⓘ

MMP↓, 1,  

Cell Death ⓘ

Apoptosis↑, 1,   Casp3↑, 1,   Casp8↑, 1,   Casp9↑, 1,   Cyt‑c↑, 1,  

DNA Damage & Repair ⓘ

cl‑PARP1↑, 1,  

Cell Cycle & Senescence ⓘ

TumCCA↑, 1,  

Immune & Inflammatory Signaling ⓘ

NF-kB↓, 1,  

Drug Metabolism & Resistance ⓘ

eff↓, 1,  

Functional Outcomes ⓘ

TumVol↓, 1,  
Total Targets: 19

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:39  Cells:%  prod#:%  Target#:1153  State#:%  Dir#:1
  wNotes=0  sortOrder:rid,rpid

 

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