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• W2079852092 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." @default.
• W2079852092 created "2016-06-24" @default.
• W2079852092 creator A5049388814 @default.
• W2079852092 creator A5059429984 @default.
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• W2079852092 date "2006-09-01" @default.
• W2079852092 modified "2023-10-16" @default.
• W2079852092 title "Ionizing radiation activates expression of FOXO3a, Fas ligand, and Bim, and induces cell apoptosis" @default.
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• W2079852092 doi "https://doi.org/10.3892/ijo.29.3.643" @default.
• W2079852092 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/2632978" @default.
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• W2079852092 hasPublicationYear "2006" @default.
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