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• W2024838090 abstract "Dexamethasone (DEX) induces apoptosis in lymphocytes, while protecting some cancer cells from apoptosis, by a poorly understood mechanism. In this study, we examined the potential role of the forkhead transcription factor (FOXO3A) in DEX-induced apoptosis. Unphosphorylated FOXO3A, the active form of FOXO3A, can translocate into nucleus and induce apoptosis. In lymphocytes, FOXO3A is upregulated by DEX treatment, while phospho-FOXO3A was downregulated. In several different types of cancer cells, we found that sensitivity to DEX correlated negatively to expression of phospho-FOXO3A. We conclude that DEX might maintain FOXO3A in its unphosphorylated, active form. Knockdown of FOXO3A expression using a small interfering RNA (siRNA) significantly reduces apoptosis in lymphocytes. This study suggests that FOXO3A has a pivotal role in DEX-induced apoptosis. Increased phospho-FOXO3A levels in cancer cells may explain, in part, their resistance to apoptosis. Therefore, FOXO3A may be a potential target for cancer therapy." @default.
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• W2024838090 date "2008-12-01" @default.
• W2024838090 modified "2023-10-15" @default.
• W2024838090 title "Glucocorticoid-induced apoptosis requires FOXO3A activity" @default.
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• W2024838090 doi "https://doi.org/10.1016/j.bbrc.2008.10.097" @default.
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