作者: Stephanie L. Lomonaco , Xiaoxin S. Xu , Gan Wang
关键词:
摘要: Many anticancer drugs target the genomic DNA of cancer cells by generating damage and inducing apoptosis. repair protects against damage–induced Although mechanisms apoptosis have been extensively studied, mechanism which prevents is not fully understood. We studied role antiapoptotic Bcl-x(L) protein in nucleotide excision (NER)–facilitated cell protection cisplatin-induced Using both normal human fibroblasts (NF) NER-defective xeroderma pigmentosum group A (XPA) G (XPG) fibroblasts, we demonstrated that a functional NER required for transcription bcl-x(l) gene. The results obtained from our Western blots revealed cisplatin treatment led to an increase level NF cells, but decrease XPA XPG cells. immunofluorescence staining indicated pathway was translocation NF-κB p65 cytoplasm into nucleus, indicative activation. Given important function regulating gene preventing apoptosis, these suggest may protect activating NF-κB, further induces gene, resulting accumulation activation survival leads increased under treatment.