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Submitted on October 25, 2004
Accepted on March 21, 2005
Kolling Institute of Medical Research, University of Sydney, Royal North Shore Hospital, St. Leonards, NSW 2065, Australia
* To whom correspondence should be addressed. E-mail: abutt{at}garvan.org.au.
Expression of IGF-binding protein (IGFBP)-3 and IGFBP-5 in human breast cancer cells induces apoptosis and is associated with modulations in Bcl-2 proteins, suggesting these IGFBPs induce an intrinsic apoptotic pathway. Here, we demonstrate that, while both IGFBPs induced the activation of caspase-8 and caspase-9, expression of IGFBP-5 but not IGFBP-3 sensitized MDA-MB-231 breast cancer cells to the inhibitory effects of TNF
. This sensitivity to TNF was associated with a block in NF
B-mediated cell survival signals. IGFBP-5 expression was also associated with a caspase-8-independent activation of Bid, increased levels of cytosolic Smac/DIABLO, and an enhanced phosphorylation of JNK, both basally and in response to TNF. These results suggest that IGFBP-5 expression may influence extrinsic apoptotic pathways via a differential modulation of downstream cell survival and cell death pathways. Furthermore, although IGFBP-3 and IGFBP-5 share much structural and functional homology, they can modulate distinct apoptotic pathways in human breast cancer cells.
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