Cell survival, DNA damage, and oncogenic transformation after a transient and reversible apoptotic response

• DOI: 10.1091/mbc.e11-11-0926
• Publication Date: 2012-04-26T20:19:57Z
• Authors: Ho Lam Tang; Ho Man Tang; Keng Hou Mak; Shaomin Hu; Shan Shan Wang; Kit Man Wong; Chung Sing Timoth...; Hoi Yan Wu; Hiu Tung Law; Kan Liu; C. Conover Talbot; Wan Keung Lau; Denise J. Montell; Ming Chiu Fung
• Keywords: HeLa

Apoptosis serves as a protective mechanism by eliminating damaged cells through programmed cell death. After apoptotic pass critical checkpoints, including mitochondrial fragmentation, executioner caspase activation, and DNA damage, it is assumed that death inevitably follows. However, this assumption has not been tested directly. Here we report an unexpected reversal of late-stage apoptosis in primary liver heart cells, macrophages, NIH 3T3 fibroblasts, cervical cancer HeLa brain cells. exposure to inducer apoptosis, exhibited multiple morphological biochemical hallmarks caspase-3 damage. Surprisingly, the vast majority dying arrested process recovered when was washed away. Of importance, some acquired permanent genetic changes underwent oncogenic transformation at higher frequency than controls. Global gene expression analysis identified molecular signature process. We propose unanticipated rescue from crisis name “anastasis” (Greek for “rising life”). Whereas carcinogenesis represents harmful side effect, potential benefits anastasis could include preservation are difficult replace stress-induced diversity.