Prostaglandin E

Elise Srour, Nathalie Martin, Claire Drullion, Clémentine De Schutter, Joëlle Giroud, Adrien Pioger, Julie Deslé, Laure Saas, Joe Nassour, Julien Théry, Gauthier Decanter, Nicolas Penel, Chantal Vercamer, Clara Salazar-Cardozo, Corinne Abbadie, Olivier Pluquet

CNRS, Inserm, CHU Lille, Institut Pasteur de Lille, UMR9020 – U1277 – CANTHER - Cancer Heterogeneity, Plasticity and Resistance to Therapies, University of Lille, Lille F-59000, France. · pubmed

Paper

Abstract

Aging of the epidermis partially occurs as a consequence of epidermal cell senescence, a non-proliferative state in which cells remain metabolically active and acquire changes in their secretome. We previously reported that senescent normal human epidermal keratinocytes (NHEKs) have two opposite outcomes: either cell death by excess of autophagic activity or escape from senescence to give rise to post-senescence neoplastic emerging (PSNE) cells. In this study, we investigated the role of PTGS2, the inducible enzyme of the prostaglandin biosynthesis pathway, in the onset of NHEK senescence and in the switch from senescence to pre-transformation. We provide evidence that the PTGS2/PGE

The following analysis is generated by AI and may contain errors. It is separate from the authors’ abstract and is not peer review.

Research summary

The paper investigates the role of PTGS2 in epidermal cell senescence and its implications for the transition to neoplastic cells, which touches on mechanisms of aging at the cellular level. However, while it addresses a specific aspect of cellular aging, the findings appear to be more focused on the pathological outcomes rather than directly targeting the root causes of aging or lifespan extension. Thus, it represents solid research but with limited broader impact on the field of longevity.

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