NDLI: BH3-only protein BIK induces caspase-independent cell death with autophagic features in Bcl-2 null cells

Content Provider	PubMed Central
Author	Rashmi, R. Pillai, Sg Vijayalingam, S. Ryerse, J. Chinnadurai, G.
Abstract	The BH3-only protein BIK normally induces apoptotic cell death. Here, we have investigated the role of BCL-2 in BIK-induced cell death using Bcl-2 +/+ and Bcl-2 −/− mouse embryo fibroblasts. Ectopic expression of BIK in Bcl-2 −/− cells resulted in enhanced cell death compared to Bcl-2 +/+ cells. In these cells, while caspase-8 was activated, there was no significant activation of caspase-9 and 3. There was no detectable mitochondrial to cytosolic release of cytochrome-c. However, there was significant redistribution of AIF from mitochondria to the nucleus. The extent of BIK-induced cell death was augmented by treatment with the pancaspase inhibitor, zVAD-fmk. The Bcl-2 null cells expressing BIK exhibited autophagic features such as cytosolic vacuoles, punctate distribution of LC3 and enhanced expression of Beclin-1. The survival of BIK-expressing Bcl-2 −/− cells was enhanced in the presence of PI3 kinase inhibitors 3-methyladenine and Wortmannin and also by depletion of Atg5 and Beclin-1. Death of BIK-expressing Bcl-2 −/− cells treated with zVAD-fmk was increased under caspase-8 depletion. Our results suggest enhanced expression of BIK in the Bcl-2 deficient cells leads to cell death with autophagic features and the extent of such cell death could be increased by inhibition of caspases.
Related Links	http://dx.doi.org/10.1038/sj.onc.1210783
Ending Page	1375
Page Count	10
Starting Page	1366
File Format	PDF
ISSN	09509232
e-ISSN	14765594
Journal	Oncogene
Issue Number	10
Volume Number	27
Language	English
Publisher Date	2008-02-28
Access Restriction	Open
Subject Keyword	Genetics Cancer Research Molecular Biology Research in Higher Education
Content Type	Text
Resource Type	Article
Subject	Genetics Molecular Biology Cancer Research

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