ZnCl(2) prevents c-myc repression and apoptosis in serum-deprived Syrian hamster embryo cells

In order to understand the c-myc implication in the apoptotic process better, we investigated the influence of ZnCl(2) on its expression in normal and transformed Syrian hamster embryo (SHE) cells in relation to apoptosis induced by serum withdrawal. Normal primary SHE cells exposed to a serum-free medium undergo rapid apoptosis characterised by a dramatic down-regulation of c-myc transcription. In these normal cells treated with ZnCl(2), c-myc expression is maintained in serum-starved conditions while apoptosis is inhibited. The results shed light on the involvement of c-myc expression in the survival of normal cells in the absence of growth factors. The regulation of c-myc expression appears to be influenced by zinc treatment as an inhibitor of apoptosis, but mechanisms sustaining the level of c-myc transcription remain to be demonstrated. The hypothesis that maintenance of c-myc expression allows cells to escape apoptosis is in accordance with results in transformed SHE cells that underwent low apoptosis and poor down-regulation of c-myc in serum-deprived conditions.