Format

Send to

Choose Destination
FEBS Lett. 2006 Jun 12;580(14):3539-44. Epub 2006 May 19.

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

Author information

1
Department of Internal Medicine, Massey Cancer Center, Virginia Commonwealth University, Medical Sciences Building 215, Richmond, 23298, USA.

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.

PMID:
16730715
DOI:
10.1016/j.febslet.2006.05.031
[Indexed for MEDLINE]
Free full text

Supplemental Content

Full text links

Icon for Wiley
Loading ...
Support Center