Autophagy delays apoptotic death in breast cancer cells following DNA damage (Cell Death and Differentiation, 2007, 14:500-510)

報告日期: 2007/11/16
報告時間: 15:10/16:00
報告學生: 吳珊瑩
講評老師: 林秋烽

Autophagy delays apoptotic death in breast cancer cells

following DNA damage

Cell Death and Differentiation (2007) 14, 500–510

Speaker : 吳珊瑩

Commentator : 林秋烽 老師

Time : 2007/11/16 15:10~16:00

Place :  Room 602

Abstract :

Stimuli, including growth factor deprivation, UV or gamma radiation and DNA-damaging agents can trigger apoptosis through an intrinsic pathway. Anti-cancer drug camptothecin treated MCF-7 cells utilize the intrinsic pathway to transduce early signaling, but the death was delayed and the cells later exhibited few hallmarks of apoptosis. CPT could induce autophagy in MCF-7 cells demonstrated under the transmission electron and confocal microscopes. Autophagy is a membrane-trafficking mechanism that delivers cytoplasmic constituents into the lysosome/vacuole for bulk protein degradation. The authors demonstrated that inhibition of autophagy unmasked a latent caspase-dependent apoptotic pathway in CPT treated MCF-7 cells and  accelerated cell death. They demonstrate that a post-mitochondrial caspase cascade is delayed as a result of early disposal of damaged mitochondria within autophagosomes. Taken together, these studies underscore a potential role for autophagy inhibitors in combination with conventional chemotherapeutic drugs in early breast cancer therapy.


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