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[Glutathione S transferases-pi]

Y Takahashi1, Y Niitsu

  • 1Dept. of Internal Medicine, Sapporo Medical University School of Medicine.

Gan to Kagaku Ryoho. Cancer & Chemotherapy
|June 1, 1994
PubMed
Summary
This summary is machine-generated.

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Glutathione S-transferase pi (GST-pi) directly contributes to anticancer drug resistance. Inhibiting GST-pi with ketoprofen partially overcomes resistance, suggesting a new therapeutic strategy for cancer treatment.

Area of Science:

  • Biochemistry
  • Molecular Biology
  • Oncology

Context:

  • Anticancer drug resistance is a major challenge in cancer therapy.
  • Glutathione S-transferase (GST) enzymes, particularly GST-pi, are implicated as potential mediators of this resistance.
  • Understanding the specific role of GST-pi is crucial for developing strategies to overcome drug resistance.

Purpose:

  • To investigate the direct relationship between GST-pi and anticancer drug resistance.
  • To explore the potential of overcoming GST-pi-mediated drug resistance.
  • To assess the efficacy of GST-pi inhibition in enhancing chemosensitivity.

Summary:

  • This study utilized antisense cDNA transfection to reduce GST-pi levels in a human colonic cancer cell line (M 7609).
  • Reduced GST-pi expression led to increased sensitivity to adriamycin, confirming GST-pi's direct role in anticancer drug resistance.

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  • Ketoprofen, a GST-pi inhibitor, also enhanced adriamycin sensitivity, demonstrating partial overcoming of drug resistance.

    • Impact:

    • The findings confirm GST-pi as a direct contributor to anticancer drug resistance, specifically against adriamycin.
    • GST-pi inhibitors represent a promising therapeutic avenue for overcoming drug resistance in cancer treatment.
    • This research paves the way for novel combination therapies involving GST-pi inhibitors to improve patient outcomes.