作者: J J Yu , K B Lee , C Mu , Q Li , T V Abernathy
DOI: 10.3892/IJO.16.3.555
关键词: Cisplatin 、 Apoptosis 、 ERCC1 、 DNA repair 、 Molecular biology 、 Biology 、 DNA adduct 、 Nucleotide excision repair 、 Pathology 、 Cell culture 、 Cell cycle
摘要: ERCC1 is an essential gene within the nucleotide excision repair process. We studied two human ovarian carcinoma cell lines for cisplatin resistance, which differed with respect to ERCC1. The A2780/CP70 line has been extensively previously, and wild-type sequence. MCAS a recently described polymorphism at codon 118, associated approximate 50% reduction in usage. These cells did not differ p53 sequence nor mRNA induction following exposure. of was markedly reduced as compared cells. At IC50 dose each line, were less proficient cisplatin-DNA adduct than In absolute terms, repaired 3-fold much (2.7 pg/microgram DNA over 6 h vs 0.86 DNA); when expressed terms maximal load, more had increased cytosolic inactivation drug level, previously suggested be compensatory cellular response capacity. data suggest possibility that this specific polymorphism, may capacity cancer This association effected through peak production mRNA, consequent translation into protein.