Apoptosis pathways in cancer cells

The term "apoptosis pathways in cancer cells" refers to a set of canonical intracellular signaling routes—primarily the intrinsic (mitochondrial-mediated) and extrinsic (death receptor-mediated) apoptotic pathways—that regulate programmed cell death in response to cell stress, DNA damage, and external death ligands[1][3][5]. Dysregulation of these pathways underpins cancer cell survival; for example, defects in the intrinsic pathway (involving Bcl-2 family proteins, cytochrome c release, and caspase activation) or extrinsic pathway (involving receptors such as TNFR1, Fas, DR4/5, and downstream caspases) allow malignant cells to evade apoptosis[1][3][4][5]. While individual components (e.g., Bcl-2, caspases, p53, death receptors) are directly druggable targets, the term "apoptosis pathways" designates a broad and complex network, not a single molecular entity. Key points: - This entry names a signaling network rather than a single receptor, enzyme, or protein. - There is no standardized abbreviation or canonical form for this "target". - Multiple druggable proteins exist within these pathways (such as Bcl-2 family proteins, caspases, or death receptors), but "apoptosis pathways in cancer cells" is not itself a molecular target. - For structured drug discovery or pharmacological targeting, refer to discrete components (e.g., "B-cell lymphoma 2 protein (Bcl-2)", "Caspase-3", "Tumor necrosis factor receptor 1 (TNFR1)", "p53 tumor suppressor protein"). If you need structured information about specific targets within the apoptosis pathways (such as Bcl-2, caspases, or death receptors), please specify the exact molecule or protein.

Other names

Apoptotic pathwaysProgrammed cell death pathwaysCell death signaling pathways