Hijacking Homeostasis: Regulation of the Tumour Microenvironment by Apoptosis

Christopher D Gregory*

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

Abstract / Description of output

Cancers are genetically-driven, rogue tissues which generate dysfunctional, obdurate organs by hijacking normal, homeostatic programmes. Apoptosis is an evolutionarily conserved regulated cell death programme and a profoundly important homeostatic mechanism that is common (alongside tumour cell proliferation) in actively growing cancers, as well as in tumours responding to cytotoxic anti-cancer therapies. Although well known for its cell-autonomous tumour-suppressive qualities, apoptosis harbours pro-oncogenic properties which are deployed through non-cell-autonomous mechanisms and which generally remain poorly defined. Here, the roles of apoptosis in tumour biology are reviewed, with particular focus on the secreted and fragmentation products of apoptotic tumour cells and their effects on tumour associated macrophages, key supportive cells in the aberrant homeostasis of the tumour microenvironment. Historical aspects of cell loss in tumour growth kinetics are considered and the impact (and potential impact) on tumour growth of apoptotic-cell clearance (efferocytosis) as well as released soluble and extracellular vesicle-associated factors are discussed from the perspectives of inflammation, tissue repair and regeneration programmes. An ‘apoptosis-centric’ view is proposed in which dying tumour cells provide an important platform for intricate intercellular communication networks in growing cancers. The perspective has implications for future research and for improving cancer diagnosis and therapy.

Original languageEnglish
JournalImmunological reviews
DOIs
Publication statusPublished - 8 Aug 2023

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