Inducing death in tumor cells: roles of the inhibitor of apoptosis proteins

The heterogeneous group of diseases collectively termed cancer results not just from aberrant cellular proliferation but also from a lack of accompanying homeostatic cell death. Indeed, cancer cells regularly acquire resistance to programmed cell death, or apoptosis, which not only supports cancer p...

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Bibliographic Details
Published inF1000 research Vol. 6; p. 587
Main Authors Finlay, Darren, Teriete, Peter, Vamos, Mitchell, Cosford, Nicholas D P, Vuori, Kristiina
Format Journal Article
LanguageEnglish
Published England Faculty of 1000 Ltd 2017
F1000Research
F1000 Research Ltd
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Summary:The heterogeneous group of diseases collectively termed cancer results not just from aberrant cellular proliferation but also from a lack of accompanying homeostatic cell death. Indeed, cancer cells regularly acquire resistance to programmed cell death, or apoptosis, which not only supports cancer progression but also leads to resistance to therapeutic agents. Thus, various approaches have been undertaken in order to induce apoptosis in tumor cells for therapeutic purposes. Here, we will focus our discussion on agents that directly affect the apoptotic machinery itself rather than on drugs that induce apoptosis in tumor cells indirectly, such as by DNA damage or kinase dependency inhibition. As the roles of the Bcl-2 family have been extensively studied and reviewed recently, we will focus in this review specifically on the inhibitor of apoptosis protein (IAP) family. IAPs are a disparate group of proteins that all contain a baculovirus IAP repeat domain, which is important for the inhibition of apoptosis in some, but not all, family members. We describe each of the family members with respect to their structural and functional similarities and differences and their respective roles in cancer. Finally, we also review the current state of IAPs as targets for anti-cancer therapeutics and discuss the current clinical state of IAP antagonists.
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These authors contributed equally
Competing interests: No competing interests were disclosed.
ISSN:2046-1402
2046-1402
DOI:10.12688/f1000research.10625.1