The Apoptosis Paradox in Cancer

Research output: Contribution to journalArticlepeer-review

Abstract

Cancer growth represents a dysregulated imbalance between cell gain and cell loss, where the rate of proliferating mutant tumour cells exceeds the rate of those that die. Apoptosis, the most renowned form of programmed cell death, operates as a key physiological mechanism that limits cell population expansion, either to maintain tissue homeostasis or to remove potentially harmful cells such as those that have sustained DNA damage. Paradoxically, high-grade cancers are generally associated with high constitutive levels of apoptosis. In cancer, cell-autonomous apoptosis constitutes a common tumour suppressor mechanism, a property which is exploited in cancer therapy. By contrast, limited apoptosis in the tumour-cell population also has the potential to promote cell survival and resistance to therapy by conditioning the tumour microenvironment (TME) – including phagocytes and viable tumour cells – and engendering pro-oncogenic effects. Notably, the constitutive apoptosis-mediated activation of cells of the innate immune system can help orchestrate a pro-oncogenic TME and may also mediate evasion of cancer treatment. Here we present an overview of the implications of cell death programmes in tumour biology, with particular focus on apoptosis as a process with “double-edged” consequences: on the one hand being tumour suppressive through deletion of pre-malignant cells, while on the other being tumour progressive through stimulation of reparatory and regenerative responses in the TME.
Original languageEnglish
Pages (from-to)1328
JournalInternational Journal of Molecular Sciences
Volume23
Issue number3
DOIs
Publication statusPublished - 25 Jan 2022

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