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p38-MAP kinase activation followed by BIM induction is essential for glucocorticoid-induced apoptosis in lymphoblastic leukemia cells.

Authors
Type
Published Article
Journal
FEBS Letters
0014-5793
Publisher
Wiley Blackwell (John Wiley & Sons)
Publication Date
Volume
580
Issue
14
Pages
3539–3544
Identifiers
PMID: 16730715
Source
Medline
License
Unknown

Abstract

Glucocorticoids (GC) are common components in chemotherapeutic protocols for lymphoid malignancies. GC-induced apoptosis requires the intrinsic, BCL-2 family-regulated pathway. Treatment of CCRF-CEM (T cell acute lymphoblastic leukemia) cells with the GC, dexamethasone (Dex), activates p38-mitogen activated protein kinase (p38-MAPK) and then induces mRNA transcription and synthesis levels of BIM, a BH3-only pro-apoptotic BCL-2 family member. Dex-induced apoptosis is dramatically inhibited by downregulation of BIM by shRNA or by pretreatment with a p38-MAPK inhibitor, SB203580, which also reduces BIM induction. These findings indicate that BIM induction through p38-MAPK activation is a critical pathway in GC-induced cell death.

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