leotide Excision Repair Gene Expression after Cisplatin

Downlo of the hallmark features of melanoma are its development as a result of chronic UV radiation exposure e limited efficacy of cisplatin in the disease treatment. Both of these DNA-damaging agents result in elix-distorting DNA damage that is recognized and repaired by nucleotide excision repair (NER). The this study was to examine the expression of NER gene transcripts, p53, and p21 in melanoma cell lines d with cisplatin compared with melanocytes. Basal expression of all genes was greater in the melanoma es compared with melanocytes. Global genome repair (GGR) transcripts showed significantly decreased e expression (RE) in melanoma cell lines 24 hours after cisplatin treatment. The basal RE of p53 was cantly higher in the melanoma cell lines compared with the melanocytes. However, induction of p53 was ignificant in the melanocytes at 6 and 24 hours after cisplatin treatment. Inhibition of p53 expression cantly decreased the expression of all the GGR transcripts in melanocytes at 6 and 24 hours after cistreatment. Although the RE levels were lower with p53 inhibition, the induction of the GGR genes was milar to that in the control melanocytes and increased significantly across the time points. The findings his study revealed reduced GGR transcript levels in melanoma cells 24 hours after cisplatin treatment. from t Our findings suggest a possible mechanistic explanation for the limited efficacy of cisplatin treatment and the possible role of UV light in melanoma. Cancer Res; 70(20); 7918–26. ©2010 AACR.