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Spectrophotometric Screening for Potential Inhibitors of Cytosolic Glutathione S-Transferases
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Spectrophotometric Screening for Potential Inhibitors of Cytosolic Glutathione S-Transferases

Published on: October 10, 2020

Glutathione S-transferases in kidney and urinary bladder tumors

Tatjana Simic1, Ana Savic-Radojevic, Marija Pljesa-Ercegovac

  • 1Institute of Medical and Clinical Biochemistry, University of Belgrade, Pasterova 2, Belgrade 11000, Serbia. tatjanasimic@med.bg.ac.rs

Nature Reviews. Urology
|May 9, 2009
PubMed

Insights

Glutathione S-transferases (GSTs) detoxify carcinogens. Genetic variations in GSTs, like GSTM1-null, increase cancer risk for kidney and bladder tumors, while others like GSTP1 are still debated.

Area of Science:

  • Biochemistry
  • Molecular Biology
  • Oncology

Background:

  • Glutathione S-transferases (GSTs) are crucial enzymes for cellular protection against carcinogens and oxidative stress.
  • Genetic polymorphisms in GST enzymes, particularly GSTM1, GSTT1, and GSTP1, can impair their detoxification activity.
  • These polymorphisms are implicated in the etiology of renal cell carcinoma (RCC) and transitional cell carcinoma (TCC).

Purpose of the Study:

  • To investigate the role of GST polymorphisms in susceptibility to RCC and TCC.
  • To explore the impact of GST enzyme expression and activity on cancer development and progression.
  • To clarify the controversial roles of specific GST polymorphisms in urinary tract cancers.

Main Methods:

  • Analysis of allelic variations in GST gene classes (GSTM, GSTT, GSTP).
  • Assessment of enzyme activity and expression levels in cancer tissues.
  • Correlation of specific genotypes (e.g., GSTM1-null, GSTT1-null, GSTP1-Ile105/Ile105) with cancer risk and phenotype.

Main Results:

  • GSTM1 and GSTT1 polymorphisms influence RCC susceptibility based on chemical exposure.
  • The GSTM1-null genotype is associated with an increased risk of TCC.
  • Decreased GSTA expression is observed during RCC development, promoting a pro-oxidant environment.
  • Upregulation of GSTT1 and GSTP1 occurs in TCC, potentially inhibiting apoptosis and promoting tumor growth.

Conclusions:

  • GST polymorphisms play a significant role in the susceptibility and progression of RCC and TCC.
  • Specific GST genotypes, like GSTM1-null, are clear risk factors for TCC.
  • Altered GST expression patterns in cancer cells contribute to tumorigenesis and may represent therapeutic targets.

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