Abstract
Most members of the death receptor family including CD95 (APO-1/Fas) have been shown to induce both apoptosis as well as non-apoptotic pathways depending on the tissue and the circumstances. One of the non-apoptotic pathways emanating from CD95, activation of NF-κB, has recently been demonstrated to regulate invasiveness of apoptosis resistant tumor cells. In contrast, activation of NF-κB in apoptosing cells is believed to be suppressed due to cleavage of various NF-κB pathway components by active caspases that execute apoptosis. We now present data demonstrating that in certain highly CD95 apoptosis sensitive cells NF-κB is robustly activated. In fact overexpression of apoptosis inhibitors such as Bcl-2 or c-FLIPL in these cells results in decreased activation of NF-κB through CD95. We propose a model in which NF-κB is generally activated in certain cells but may have different functions depending on whether cells are programmed to die or to survive.
Original language | English (US) |
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Pages (from-to) | 1235-1239 |
Number of pages | 5 |
Journal | Cell Cycle |
Volume | 3 |
Issue number | 10 |
DOIs | |
State | Published - Oct 2004 |
Keywords
- Bcl-2
- Fas
- Invasiveness
- NF-κB
- c-FLIP
ASJC Scopus subject areas
- Molecular Biology
- Cell Biology
- Developmental Biology