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Rosiglitazone reverses mitomycin C resistance in human gastric cancer cells

Li Zhang1, Jian-Feng Hu, Guo-Qing Li

  • 1Department of Gastroenterology, The Second Affiliated Hospital, University of South China, Hengyang, Hunan, China.

The American Journal of the Medical Sciences
|November 5, 2011
PubMed
Abstract

Insights

Rosiglitazone (ROS) reverses mitomycin C (MMC) resistance in gastric cancer cells by reducing key drug resistance proteins and increasing apoptosis. This study explores ROS mechanisms in overcoming drug resistance in human gastric cancer.

Area of Science:

  • Oncology
  • Pharmacology
  • Molecular Biology

Background:

  • Gastric cancer exhibits resistance to chemotherapy, necessitating novel therapeutic strategies.
  • Drug resistance mechanisms, including overexpression of efflux pumps and anti-apoptotic proteins, limit treatment efficacy.
  • Peroxisome proliferator-activated receptor gamma (PPARγ) ligands are being investigated for their role in cancer therapy.

Purpose of the Study:

  • To investigate the mechanisms by which rosiglitazone (ROS), a PPARγ ligand, reverses mitomycin C (MMC) resistance in a human drug-resistant gastric cancer cell line.
  • To evaluate the impact of ROS on apoptosis and the expression of key drug resistance markers.

Main Methods:

  • Utilized a human drug-resistant gastric cancer cell line (SGC7901/VCR) and its parental line (SGC7901).
  • Assessed drug sensitivity using a tetrazolium blue (MTT) assay.
  • Determined apoptosis induction via flow cytometry and acridine orange-ethidium bromide staining.
  • Quantified mRNA and protein expression of multidrug resistant 1 (MDR1), Livin, and P-glycoprotein (P-gp) using RT-PCR and Western blotting.

Main Results:

  • Rosiglitazone (ROS) dose-dependently increased the reversal index in MMC-treated SGC7901/VCR cells.
  • ROS treatment significantly enhanced MMC-induced apoptosis in resistant cells.
  • Elevated mRNA levels of MDR1 and Livin, and protein levels of P-gp were observed in SGC7901/VCR cells compared to parental cells.
  • ROS treatment, alone or combined with MMC, markedly modulated the expression of MDR1, Livin, and P-gp in resistant cells.

Conclusions:

  • Rosiglitazone (ROS) effectively reverses mitomycin C (MMC) resistance in human gastric cancer SGC7901/VCR cells.
  • The mechanism involves the reduction of multidrug resistance 1 (MDR1), Livin, and P-glycoprotein (P-gp) expression.
  • ROS enhances apoptosis, contributing to overcoming drug resistance in gastric cancer.

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