title: Apoptotic Caspases in Promoting Cancer: Implications from Their Roles in Development and Tissue Homeostasis.
abstract: 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.
authors: School of Biosciences, University of Birmingham, Edgbaston, Birmingham, B15 2TT, UK.
authors: Catherine
authors: C
authors: Dabrowska
authors: School of Biosciences, University of Birmingham, Edgbaston, Birmingham, B15 2TT, UK.
authors: Mingli
authors: M
authors: Li
authors: School of Biosciences, University of Birmingham, Edgbaston, Birmingham, B15 2TT, UK. y.fan@bham.ac.uk.
authors: Yun
authors: Y
authors: Fan
mesh_terms: D000818:Animals; D000970:Antineoplastic Agents / Q000494:pharmacology / Q000627:therapeutic use; D017209:Apoptosis / Q000502:physiology*; D017173:Caenorhabditis elegans / Q000502:physiology; D029742:Caenorhabditis elegans Proteins / Q000502:physiology; D063646:Carcinogenesis; D020169:Caspases / Q000502:physiology*; D002455:Cell Division; D004249:DNA Damage; D029721:Drosophila Proteins / Q000502:physiology; D004331:Drosophila melanogaster / Q000502:physiology; D006706:Homeostasis; D006801:Humans; D008322:Mammals / Q000502:physiology; D008938:Mitosis; D009362:Neoplasm Metastasis; D009363:Neoplasm Proteins / Q000502:physiology*; D009369:Neoplasms / Q000201:enzymology* / Q000473:pathology / Q000503:physiopathology; D053218:Receptors, Death Domain / Q000502:physiology; D015398:Signal Transduction / Q000502:physiology
chemical_list: D000970:Antineoplastic Agents; D029742:Caenorhabditis elegans Proteins; D029721:Drosophila Proteins; D009363:Neoplasm Proteins; D053218:Receptors, Death Domain; D020169:Caspases
keywords: Apoptosis; Apoptosis-induced proliferation; Cancer; Caspase; Development; Non-apoptotic function; Tissue homeostasis