The apoptotic effects of cisplatin and carboplatin in retinoblastoma Y79 cells.
Cell Survival
Retinoblastoma
Antineoplastic Agents
Apoptosis
DNA, Neoplasm
Carboplatin
3. Good health
03 medical and health sciences
0302 clinical medicine
Proto-Oncogene Proteins c-bcl-2
Drug Resistance, Neoplasm
carboplatin
Tumor Cells, Cultured
Humans
Cisplatin
Tumor Suppressor Protein p53
DOI:
10.3892/ijo.13.2.225
Publication Date:
2014-03-10T07:24:39Z
AUTHORS (6)
ABSTRACT
This study demonstrated that cisplatin and carboplatin stimulate apoptosis in human retinoblastoma Y79 cells, cisplatin being the most effective compound. The apoptotic effect appeared after 8 h and then increased in a time-dependent manner. Treatment with cisplatin and carboplatin also provoked an increase in the level of p53 and p21, and a lowering in Bcl-2. The prolonged exposure of Y79 cells to cisplatin induced resistance to cisplatin, carboplatin and etoposide. The basal level of p53 was in resistant cells higher than in untreated cells, while Bcl-2 was not modified. p53 and Bcl-2 levels did not change after treating of resistant cells with cisplatin, carboplatin or etoposide. However, camptothecin which is a powerful inducer of apoptosis in sensitive cells, triggered cell death even in resistant cells. Such an effect was not accompanied by any modification in p53 level while Bcl-2 was markedly reduced.
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