Concordance between tumour cell activation by epidermal growth factor and alteration of cell sensitivity to cisplatin and lymphokine-activated killer cell activity.
- A M Nouri
- S T Zubairi
- M V Russell
- T Moss
- H Cannell
- A M Paris
- M Symes
- R T Oliver
Affiliations: London Hospital Medical College, Whitechapel, London E1 1BB, UK.
- Published online on: January 1, 2000 https://doi.org/10.3892/or.7.1.197
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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.