One of the main mechanisms the body uses to protect itself against cancer is to switch off defective cells by making them senescent; these cells do not die but stop dividing: their life cycle stops. A team of researchers from the Spanish National Cancer Research Centre (CNIO) in Madrid and another one from the Centre for Genomic Regulation (CRG) in Barcelona have discovered, and are publishing in two articles in the journal Cell, that this switching-off mechanism also takes place in embryos, and not as a response to cell damage but as part the normal process of development. As the embryo grows, and its tissues change shape and function, senescence switches off cells that are no longer necessary. These switched-off cells are later on recognized and eliminated by a special type of cells of the immune system known as macrophages. The occurrence of senescence during embryonic development has important implications for understanding how the body grows and is shaped.
"We have discovered that cellular senescence is a tissue remodelling mechanism during embryo development", says Manuel Serrano, head of CNIO's Tumour Suppression Group and leader of the study, whose first author is Daniel Muoz-Espn. "Embryo development is full of recycling: tissues with one function at one point in the process are used for something different further down the line; in this redesigning process, there are cells that are no longer needed, and one way of getting rid of them is to make them senescent". The CRG study was led by Bill Keyes, and the first author is Mekayla Storer.
Senescence is one of the most studied cellular processes because of its relationship to cancer and ageing. It is often presented as a double-edged sword: both as protection against cancer and for its important role in the ageing of the body. The authors of the present study, however, warn against the simplistic idea that ageing is a consequence of senescence. "In my opinion, senescence is a fundamentally
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Centro Nacional de Investigaciones Oncologicas (CNIO)