Abstract:
:Genotoxic stress such as ionizing radiation can induce DNA damage and promote cell-cycle arrest or apoptosis through either a p53-dependent or -independent pathway. Recently, members of the FOXO Forkhead transcription factor family have been implicated in playing a role in both DNA repair and apoptosis in mammalian cells that promoted us to examine the role of FOXO transcription factors in ionizing radiation-induced apoptosis. Here, we show that ionizing radiation can promote FOXO3a (FKHRL1) transcriptional activity and protein expression level, and induce nuclear translocation of FOXO3a in Saos2, a p53-null osteosarcoma cell line. Ionizing radiation stimulates expression of apoptosis-inducing proteins such as Fas ligand and the Bcl-2 interacting mediator of cell death (Bim) leading to cellular apoptosis. The observed upregulation of proapoptotic genes and apoptosis in cells without p53 in response to ionizing radiation suggests a novel p53-independent mechanism underlying ionizing radiation-induced apoptosis in cancer cells.
journal_name
Int J Oncoljournal_title
International journal of oncologyauthors
Yang JY,Xia W,Hu MCsubject
Has Abstractpub_date
2006-09-01 00:00:00pages
643-8issue
3eissn
1019-6439issn
1791-2423journal_volume
29pub_type
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journal_title:International journal of oncology
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pub_type: 杂志文章,评审
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journal_title:International journal of oncology
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