Apoptoz ve Nekroz Dışındaki Hücre Ölüm Mekanizmaları ve Kanser İle İlişkileri
Synopsis
This study examines regulated cell death mechanisms other than apoptosis and necrosis and their complex relationships with cancer. According to the criteria of the Nomenclature Committee on Cell Death (NCCD), cell death relies on genetically controlled molecular regulations in physiological and pathological processes. As the traditional tripartite classification proved insufficient, new forms such as anoikis, MPT-driven necrosis, necroptosis, ferroptosis, pyroptosis, parthanatos, entotic cell death, NETotic cell death, lysosome-dependent, and autophagy-dependent cell death have been introduced to the literature. Induced by the disruption of cell-extracellular matrix interactions, anoikis is particularly associated with tumor metastasis and anoikis resistance; meanwhile, ferroptosis—developing through iron-dependent lipid peroxidation and GSH/GPX4 depletion—plays a critical role in the pathophysiology of various cancer types including pancreatic, liver, gastric, breast, and lung cancers. Necroptosis, progressing via the activation of RIPK1, RIPK3, and MLKL, leads to the release of inflammatory DAMPs, whereas pyroptosis, triggered by gasdermin D pores and caspases-1/4/5/11, mediates innate immune responses. Other processes, such as parthanatos—which causes a bioenergetic crisis resulting from PARP1 hyperactivation—as well as entosis driven by cellular invasion and NETosis defined by neutrophil extracellular traps, contribute to tissue homeostasis. Consequently, elucidating these alternative cell death pathways in detail is of vital importance for understanding cancer cell evasion mechanisms and developing innovative target-oriented therapeutic strategies.
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