Target intelligence / Profile preview

Glutathione S-transferase mu 3 (GSTM3)

Target
GSTM3
Molecular classification
Enzyme, Phase II detoxification enzyme, Glutathione S-transferase (mu class)
01

Overview

Glutathione S-transferase mu 3 (GSTM3) is a cytosolic phase II detoxification enzyme of the glutathione S-transferase (GST) superfamily (mu class), mainly functioning to catalyze the conjugation of reduced glutathione to a broad spectrum of endogenous and exogenous electrophilic compounds, including carcinogens, drugs, and environmental toxins. GSTM3 helps protect cells from oxidative and chemical stress and is expressed in various tissues (notably brain, liver, and testis). The gene is polymorphic, and these genetic variants can alter individual susceptibility to environmental toxins and carcinogens and modify drug response and toxicity, especially in the context of chemotherapy. Deregulation of GSTM3 is associated with various cancers and their progression, as well as variability in prognosis and therapeutic outcomes. In cancer biology, GSTM3 modulates processes such as ferroptosis and is being explored as a therapeutic and prognostic biomarker, particularly in treatment-resistant malignancies.

Other names
GSTM3GST5hGSTM3-3GST class-mu 3GSTM3-3GSTM3TV2GSTBGTM3S-(hydroxyalkyl)glutathione lyase M3brain GSTbrain type mu-glutathione S-transferaseepididymis secretory sperm binding proteinglutathione S-alkyltransferase M3glutathione S-aralkyltransferase M3glutathione S-aryltransferase M3
02

Mechanism of action

Glutathione conjugation: catalyzes the conjugation of glutathione to electrophilic compounds for detoxification; Modulation of oxidative stress and drug metabolism; Influences ferroptosis response in certain resistant cancers, which can be targeted through combination with ferroptosis-inducing drugs and radiotherapy.

03

Biological functions

Detoxification of electrophilic compounds (xenobiotics, carcinogens, therapeutic drugs, toxins, products of oxidative stress) by conjugation with reduced glutathioneCellular defense against oxidative and chemical stressRegulation of susceptibility to carcinogens and toxinsInvolvement in drug metabolism and eliminationModulation of ferroptosis (in specific cancer contexts)Protein homodimerization
04

Disease associations

Cancer (including hepatocellular carcinoma, pancreatic cancer, colorectal cancer, breast cancer, lung cancer, prostate cancer, glioma)Pharmacogenomic toxicity (influences response and side effects of chemotherapy drugs)Environmental toxin susceptibility (e.g., increased risk of cancer with certain polymorphisms)Immune response modulation (implicated in occupational asthma)Poor prognosis and tumor progression (when downregulated or mutated in certain tumors)
05

Safety considerations

Genetic polymorphisms influencing drug response and toxicityLoss of GSTM3 function or aberrant expression linked to increased cancer risk and worse disease outcomes
06

Interacting drugs

No specific therapeutic drugs directly listed as GSTM3-targeted, but its activity modulates response/toxicity of various chemotherapeutic agents (e.g., cisplatin, environmental carcinogens)
07

Biomarkers

GSTM3 expression as a potential biomarker for radioresistance, prognosis, and susceptibility to xenobiotic-induced diseases

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