NDLI: The inhibitors of apoptosis (IAPs) as cancer targets

Content Provider	Springer Nature Link
Author	Hunter, Allison M. LaCasse, Eric C. Korneluk, Robert G.
Copyright Year	2007
Abstract	Apoptosis has been accepted as a fundamental component in the pathogenesis of cancer, in addition to other human diseases including neurodegeneration, coronary disease and diabetes. The origin of cancer involves deregulated cellular proliferation and the suppression of apoptotic processes, ultimately leading to tumor establishment and growth. Several lines of evidence point toward the IAP family of proteins playing a role in oncogenesis, via their effective suppression of apoptosis. The central mechanisms of IAP apoptotic suppression appear to be through direct caspase and pro-caspase inhibition (primarily caspase 3 and 7) and modulation of, and by, the transcription factor NF-kappaB. Thus, when the IAPs are over-expressed or over-active, as is the case in many cancers, cells are no longer able to die in a physiologically programmed fashion and become increasingly resistant to standard chemo- and radiation therapies. To date several approaches have been taken to target and eliminate IAP function in an attempt to re-establish sensitivity, reduce toxicity, and improve efficacy of cancer treatment. In this review, we address IAP proteins as therapeutic targets for the treatment of cancer and emphasize the importance of novel therapeutic approaches for cancer therapy. Novel targets of IAP function are being identified and include gene therapy strategies and small molecule inhibitors that are based on endogenous IAP antagonists. As well, molecular mechanistic approaches, such as RNAi to deplete IAP expression, are in development.
Starting Page	1543
Ending Page	1568
Page Count	26
File Format	PDF
ISSN	13608185
Journal	Apoptosis
Volume Number	12
Issue Number	9
e-ISSN	1573675X
Language	English
Publisher	Kluwer Academic Publishers-Plenum Publishers
Publisher Date	2007-06-19
Publisher Place	New York
Access Restriction	One Nation One Subscription (ONOS)
Subject Keyword	Apoptosis Cancer IAPs Caspases Smac NFkB TNFR TRAF Knock out mice Virology Biochemistry Oncology Cell Biology Cancer Research
Content Type	Text
Resource Type	Article
Subject	Pharmaceutical Science Biochemistry (medical) Cell Biology Clinical Biochemistry Cancer Research Pharmacology

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