Tumor cell death pathway

Tumor cell death pathways" is not a single molecule or receptor but rather refers collectively to the various regulated mechanisms by which tumor cells undergo programmed or non-programmed forms of cellular demise. These include apoptosis (intrinsic and extrinsic), necroptosis, ferroptosis, autophagy-dependent cell death, pyroptosis, and others. Each pathway involves distinct molecular machinery: **Apoptosis** can be triggered via intrinsic signals (mitochondrial pathway involving BAX/BAK and cytochrome c release) or extrinsic signals (death receptor-mediated activation via TNFR1, FAS/CD95/APO1, TRAIL-R). Both converge on caspase activation leading to orderly cellular dismantling[1][2]. **Necroptosis** is a form of regulated necrosis dependent on RIPK1/RIPK3/MLKL signaling when caspase activity is inhibited[1]. **Ferroptosis** involves iron-dependent lipid peroxidation. **Autophagy**, while primarily a survival mechanism under stress conditions through degradation and recycling of cellular components, can also lead to autophagic cell death in certain contexts; its role in cancer is complex—sometimes suppressing tumor initiation but often promoting survival in established tumors[4]. Other forms like **pyroptosis**, mediated by inflammasome activation and gasdermin D cleavage resulting in inflammatory lytic cell death, are also relevant. These pathways are frequently dysregulated in cancer cells as part of their evasion strategies against therapy-induced cytotoxicity. Therapeutic targeting typically focuses on modulating specific proteins within these cascades (e.g., BCL2 family for apoptosis; RIPK3 for necroptosis), not the entire "pathway" as an undifferentiated target. Thus "tumor cell death pathways" should not be considered a canonical therapeutic target itself but rather an umbrella term encompassing several actionable molecular targets within each pathway[1][4].

Other names

Regulated cell death pathwaysCancer cell death pathwaysProgrammed cell death in cancer