Apoptosis Cascade Disruption

Apoptosis is a tightly regulated process of programmed cell death essential for development, tissue homeostasis, and immune regulation. Disruption of this cascade, particularly through anti-apoptotic mechanisms, prevents or delays cell death. Key pathways involved include the intrinsic (mitochondrial) pathway (Bcl-2 family regulation) and the extrinsic (death receptor) pathway. Disrupting apoptosis cascades typically involves overexpression or hyperactivation of anti-apoptotic proteins (e.g., Bcl-2, Bcl-xL, IAPs), downregulation/inhibition/mutation in pro-apoptotic factors (e.g., Bax/Bak), or impairment in p53 function. Anti-apoptotic effects can result in enhanced survival under conditions that would normally trigger apoptosis and resistance to chemotherapy/radiation therapy in cancer. Targeting molecules involved in apoptosis disruption is a major strategy for cancer therapy. Pro-apoptotic drugs aim to inhibit anti-apoptotic proteins or restore function/losses elsewhere in the pathway. Conversely, some therapies seek transient protection from apoptosis during acute injury.

Other names

Anti-apoptotic effectInhibition of apoptosisApoptosis evasion

Inhibition of pro-apoptotic proteins, upregulation of anti-apoptotic proteins.