Expression of a resistance mechanism in ovarian and cervical carcinoma cells prevents their lysis by gamma-interferon

Cancer Res. 1990 Aug 15;50(16):4923-8.

Abstract

Despite extensive evidence that recombinant human gamma-interferon (IFN-gamma) exerts antiproliferative effects on a variety of cancer cell lines, IFN-gamma has not been shown to lyse cells in vitro. In order to determine whether some cancer cells might actively resist lysis by IFN-gamma, we examined eight arbitrarily selected cell lines derived from gynecological malignancies (ME-180, MS751, HT-3, SiHa, and C-33A human cervical carcinoma lines; Caov-3, SK-OV-3, and NIH:OVCAR-3 human ovarian carcinoma cell lines) for lysis by IFN-gamma. In a 24-h assay involving release of 51Cr from cells, none of these cell lines was lysed by IFN-gamma, either alone or in combination with actinomycin-D or emetine, two inhibitors of protein synthesis. However, pretreatment of cells with 100 units/ml of IFN-gamma for 24 h, followed by inhibition of protein synthesis, led to significantly increased lysis of the cell lines ME-180, MS751, and Caov-3. These results indicate that IFN-gamma induces a lytic mechanism in some cancer cells that is opposed by a protein synthesis-dependent resistance mechanism. This suggests that a combination therapy involving IFN-gamma and inhibitors of protein synthesis may be useful in the treatment of some cancers.

MeSH terms

  • Cell Line
  • Cell Survival / drug effects*
  • Dactinomycin / pharmacology
  • Drug Resistance
  • Emetine / pharmacology
  • Female
  • Humans
  • Interferon-gamma / pharmacology*
  • Kinetics
  • Ovarian Neoplasms
  • Recombinant Proteins
  • Time Factors
  • Tumor Cells, Cultured / cytology*
  • Tumor Cells, Cultured / drug effects
  • Uterine Cervical Neoplasms

Substances

  • Recombinant Proteins
  • Dactinomycin
  • Interferon-gamma
  • Emetine