A New Pathway of Chemotherapy Induced Apoptosis in a Prostate Cancer Cell Line
Abstract
A current view is that cytotoxic stress, such as DNA damage, induces apoptosis by regulating permeability of mitochondria. Mitochondria sequester several proteins that, if released, kill by activating caspases, the proteases that disassemble the cell. Another way to activate caspases, which is used by cytokines, is to assemble receptor complexes that activate caspases directly, although the subsequent mitochondrial permeabilization accelerates cell disassembly by amplifying caspase activity. We found that cytotoxic stress causes activation of caspase-2 and that this caspase is required for permeabilization of mitochondria. Therefore, we argue that cytokine and stress-induced apoptosis act through conceptually similar pathways in which mitochondria are amplifiers of caspase activity rather than initiators of caspase activation.
Document Details
- Document Type
- Technical Report
- Publication Date
- Jun 01, 2002
- Accession Number
- ADA410309
Entities
People
- Patrice Lassus
- Ximena Opitz-araya
- Yuri A. Lazebnik
Organizations
- Cold Spring Harbor Laboratory