Concordance between tumour cell activation by epidermal growth factor and alteration of cell sensitivity to cisplatin and lymphokine-activated killer cell activity

Oncol Rep. 2000 Jan-Feb;7(1):197-201.

Abstract

In this study the impact of epidermal growth factor (EGF) on chemosensitivity and susceptibility to lymphokine-activated killer (LAK) cytolysis on six cell lines (one super expressing EGFr i.e. HN5, three high expressing i.e. Hep2, KB and MCF-7 and two low expressing i.e. Fen and HN15) was investigated using the tetrazolium salt reduction assay (MTT) as measured by optical density (OD). Hep2, KB, MCF-7 and Fen lines showed a dose-related inhibition to cisplatin (from 19% to 80%). Treatment of EGFr positive cell lines, Hep2, KB and MCF-7 but not EGFr negative Fen by EGF prior to exposure to cisplatin inhibited the cells by between 10-15% (p<0.05). Exposure of HN5 line to EGF (0.1 ng/ml) prior to LAK assay, led to a decrease in tumour killing (13%, p<0.05). However, at 0.01 ng/ml the pre-treatment enhanced tumour sensitivity. These data indicated that pre-exposure of tumour cells to EGF altered their response to cisplatin and LAK killing and this depended on the degree of EGFr expression. These data may prove helpful for pre-selection of patients for an appropriate therapy.

MeSH terms

  • Antineoplastic Agents / pharmacology*
  • Cisplatin / pharmacology*
  • Dose-Response Relationship, Drug
  • Epidermal Growth Factor / pharmacology*
  • Hot Temperature
  • Humans
  • Immunotherapy, Adoptive*
  • Killer Cells, Lymphokine-Activated / immunology*
  • Neoplasms / therapy*
  • Tumor Cells, Cultured

Substances

  • Antineoplastic Agents
  • Epidermal Growth Factor
  • Cisplatin