Apoptosis evasion

Apoptosis evasion describes the ability of cells, especially cancer cells, to avoid programmed cell death and survive despite signals that would normally induce apoptosis. Cells evade apoptosis via dysregulation of apoptotic signaling pathways, like overexpression of anti-apoptotic proteins (e.g., BCL-2, IAP family), downregulation or mutation of pro-apoptotic proteins (e.g., BAX, Bak), abrogation of death receptor signaling (extrinsic pathway), and interference with caspase activation. This enables the survival and proliferation of damaged or transformed cells, contributing directly to tumorigenesis, metastasis, and resistance to chemotherapy[3][4][5][7][8]. The actual therapeutic targets in "apoptosis evasion" are signaling proteins (e.g., BCL-2, IAP, death receptors) and not the evasion process itself. In summary: "Apoptosis evasion" should not be considered a drug target or molecular entity but as a pathological process. For structured information about actual drug targets, one must specify the underlying molecule(s), such as "BCL-2," "IAP family proteins," "Caspase-3," or "Fas receptor."[4][5][8]

Other names

apoptotic resistanceanti-apoptotic phenotyperesistance to apoptosisdefective apoptosis