Apoptotic caspases in promoting cancer: implications from their roles in development and tissue homeostasis

Catherine Dabrowska, MingLi Li, Yun Fan

Research output: Contribution to journalArticle

13 Citations (Scopus)
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Apoptosis, a major form of programmed cell death, is an important mechanism to remove extra or unwanted cells during development. In tissue homeostasis apoptosis also acts as a monitoring machinery to eliminate damaged cells in response to environmental stresses. During these processes, caspases, a group of proteases, have been well defined as key drivers of cell death. However, a wealth of evidence is emerging which supports the existence of many other non-apoptotic functions of these caspases, which are essential not only in proper organism development but also in tissue homeostasis and post-injury recovery. In particular, apoptotic caspases in stress-induced dying cells can activate mitogenic signals leading to proliferation of neighbouring cells, a phenomenon termed apoptosis-induced proliferation. Apparently, such non-apoptotic functions of caspases need to be controlled and restrained in a context-dependent manner during development to prevent their detrimental effects. Intriguingly, accumulating studies suggest that cancer cells are able to utilise these functions of caspases to their advantage to enable their survival, proliferation and metastasis in order to grow and progress. This book chapter will review non-apoptotic functions of the caspases in development and tissue homeostasis with focus on how these cellular processes can be hijacked by cancer cells and contribute to tumourigenesis.
Original languageEnglish
Pages (from-to)89-112
Number of pages24
JournalAdvances in Experimental Medicine and Biology
Publication statusPublished - 2016

Bibliographical note

Advances in Experimental Medicine and Biology.
Title: Apoptosis in Cancer Pathogenesis and Anti-cancer Therapy: New Perspectives and Opportunities
Editor: Christopher D. Gregory
volume 930
ISSN: 0065-2598
ISBN: 978-3-319-39404-6, 978-3-319-39406-0
DOI: 10.1007/978-3-319-39406-0


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