Source: University of California, Santa Barbara
Summary: Researchers explore the molecular underpinnings behind anastasis, a process allows the cells to recover from the verge of programmed death (apoptosis).
A team of researchers from two UC Santa Barbara labs (Denise Montell’s lab and Kosik Molecular and Cellular Neurobiology Lab) came together to explore the molecular mechanism behind the process called anastasis (Greek word = ‘’rising to life”). Based on the earlier work that cells can recover from the edge of death, this new research reveals that anastasis is an active process constitutes of two distinguishable stages. Discovering how to inhibit anastasis could enhance the effectiveness of current cancer therapies. The findings were published in the Journal of Cell Biology.
In the study, firstly, a toxin is added to the growth medium to induce apoptosis (programmed cell death, an integral part of almost every cell) and bring the cells to the edge of death. The growth medium is exchanged and the inducer is removed to allow the cells to recover for 1, 2, 3, 4, 8 or 12 hours. At every step, millions of cells were collected and their RNAs were sequenced to know how their genetic profiles changed during the process. The data from the RNA profiles not only reveals the active nature of anastasis but also its two distinct stages.
Prof. Denise Montell said, “We knew already that cells need to transcribe new genes in order to recover, so we profiled every molecule of m-RNA in the cells as they started to die and then as they recovered, Chemotherapy drugs and radiation are known to induce cancer cells to undergo apoptosis. But anastasis may give them a way to bounce back after treatment.” The researchers were further interested to better understand the earliest phases of anastasis, long-term cellular effects of anastasis and anastatic cells retaining a permanent epigenetic memory of the experience.
More information: Gongping Sun et al, A molecular signature for anastasis, recovery from the brink of apoptotic cell death, The Journal of Cell Biology (2017).DOI: 10.1083/jcb.201706134