Glucocorticoid-induced apoptosis requires FOXO3A activity.

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.

authors

Ma J,Xie Y,Shi Y,Qin W,Zhao B,Jin Y

doi

10.1016/j.bbrc.2008.10.097

subject

Has Abstract

pub_date

2008-12-19 00:00:00

pages

894-8

issue

3

eissn

0006-291X

issn

1090-2104

pii

S0006-291X(08)02044-5

journal_volume

377

pub_type

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