Malignant transformation of wild-type but not plasminogen activator inhibitor-1 gene-deficient fibroblasts decreases cellular sensitivity to chemotherapy-mediated apoptosis

Eur J Cancer. 2005 May;41(7):1095-100. doi: 10.1016/j.ejca.2005.02.010.

Abstract

Plasminogen activator inhibitor-1 (PAI-1) inhibits the activation of the plasminogen activator system, the latter being involved in cancer growth and dissemination. Interestingly, PAI-1 is elevated in many solid tumours and this elevation has consistently been shown to be associated with shorter length of patient survival. This study aims to determine whether PAI-1 contributes to cancer cell growth by inhibiting apoptosis of tumour cells. It is shown that spontaneous transformation decreases cellular sensitivity to chemotherapy-mediated apoptosis of wild-type, but not PAI-1 gene-deficient, fibrosarcomas. PAI-1 gene-deficient and wild-type mice displayed similar sensitivity to treatment with etoposide, suggesting a differential effect of PAI-1 expression between cancer cells and normal cells. Thus, since PAI-1 appears to be an important factor in regulating apoptosis in cancer cells but not in normal cells, inhibitors of PAI-1 might be useful as sensitising pre-treatment for subsequent apoptosis-inducing anti-cancer therapy.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Antineoplastic Agents, Phytogenic / pharmacology
  • Apoptosis / drug effects
  • Apoptosis / physiology*
  • Blotting, Western
  • Cell Transformation, Neoplastic
  • Dose-Response Relationship, Drug
  • Etoposide / pharmacology
  • Fibroblasts / pathology*
  • Fibrosarcoma / drug therapy
  • Fibrosarcoma / pathology*
  • Lung Neoplasms / drug therapy
  • Lung Neoplasms / pathology*
  • Male
  • Mice
  • Plasminogen Activator Inhibitor 1 / deficiency
  • Plasminogen Activator Inhibitor 1 / genetics*

Substances

  • Antineoplastic Agents, Phytogenic
  • Plasminogen Activator Inhibitor 1
  • Etoposide