Molecular signature of anastasis for reversal of apoptosis [version 1; peer review: 1 approved, 1 approved with reservations]

Apoptosis is a type of programmed cell death that is essential for normal organismal development and homeostasis of multicellular organisms by eliminating unwanted, injured, or dangerous cells. This cell suicide process is generally assumed to be irreversible. However, accumulating studies suggest that dying cells can recover from the brink of cell death. We recently discovered an unexpected reversibility of the execution-stage of apoptosis in vitro and in vivo, and proposed the term anastasis (Greek for "rising to life") to describe this cell recovery phenomenon. Promoting anastasis could in principle preserve injured cells that are difficult to replace, such as cardiomyocytes and neurons. Conversely, arresting anastasis in dying cancer cells after cancer therapies could improve treatment efficacy. To develop new therapies that promote or inhibit anastasis, it is essential to identify the key regulators and mediators of anastasis - the therapeutic targets. Therefore, we performed time-course microarray analysis to explore the molecular mechanisms of anastasis during reversal of ethanol-induced apoptosis in mouse primary liver cells. We found striking changes in transcription of genes involved in multiple pathways, including early activation of pro-survival genes, cell cycle arrest, stress-inducible responses, and at delayed times, cell migration and angiogenesis. Here, we present the time-course whole-genome gene expression dataset revealing gene expression profiles during the reversal of apoptosis. This dataset provides important insights into the physiological, pathological, and therapeutic implications of anastasis.