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Cellular senescence

In memoriam Judy Campisi: spreading cellular senescence

Nature Reviews Molecular Cell Biology (2024)Cite this article

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Cellular senescence is characterized by an irreversible proliferative arrest. It was first observed as the consequence of exhaustion of proliferative capacity (replicative cellular senescence) caused by telomere shortening associated with ageing. Cellular senescence was later found to also be induced by oncogene activation in normal cells and proposed to be a tumour-suppressive mechanism as it restrained the proliferation of cells bearing activated oncogenes. All these features are cell-autonomous, meaning that they are intrinsic to senescent cells and with an impact limited to senescent cells themselves. Our understanding of cellular senescence and its effect on organismal physiology dramatically changed with the work of Judy Campisi — the pioneer of the field of cellular senescence, who died on 19 January 2024.

The SASP was shown to promote malignant phenotypes such as epithelial–mesenchymal transition (EMT) and invasiveness in premalignant cells. These findings changed the view of cellular senescence from a cell-autonomous tumour-suppressive mechanism to a cell-non-autonomous pro-malignant role. Moreover, SASP was found to be strongest in cells undergoing oncogene-induced senescence and after p53 loss, indicating how oncogene activation and the loss of tumour suppressors can promote cancer development by cell-non-autonomous mechanisms mediated by the SASP.

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References

Original articles

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Authors and Affiliations

  1. IFOM ETS - The AIRC Institute of Molecular Oncology, Milan, Italy

    Fabrizio d’Adda di Fagagna

  2. Institute of Molecular Genetics IGM-CNR “Luigi Luca Cavalli-Sforza”, Pavia, Italy

    Fabrizio d’Adda di Fagagna

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  1. Fabrizio d’Adda di Fagagna
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Correspondence to Fabrizio d’Adda di Fagagna.

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d’Adda di Fagagna, F. In memoriam Judy Campisi: spreading cellular senescence. Nat Rev Mol Cell Biol (2024). https://doi.org/10.1038/s41580-024-00736-w

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  • DOI: https://doi.org/10.1038/s41580-024-00736-w

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