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MINI REVIEW article

Front. Cell Dev. Biol.
Sec. Cancer Cell Biology
Volume 12 - 2024 | doi: 10.3389/fcell.2024.1451274
This article is part of the Research Topic Neurodevelopmental Disorders and Cancer - Similarities and Differentiating Factors View all 3 articles

Regulation of p53 by the mitotic surveillance/stopwatch pathway: implications in neurodevelopment and cancer

Provisionally accepted
Travis H. Stracker Travis H. Stracker *
  • Radiation Oncology Branch, Center for Cancer Research, National Cancer Institute (NIH), Bethesda, Maryland, United States

The final, formatted version of the article will be published soon.

    The transcription factor p53 (encoded by TP53) plays diverse roles in human development and disease. While best known for its role in tumor suppression, p53 signaling also influences mammalian development by triggering cell fate decisions in response to a wide variety of stresses. After over 4 decades of study, a new pathway that triggers p53 activation in response to mitotic delays was recently identified. Termed the mitotic surveillance or mitotic stopwatch pathway, the USP28 and 53BP1 proteins activate p53 in response to delayed mitotic progression to control cell fate and promote genomic stability. In this Minireview, I discuss its identification, potential roles in neurodevelopmental disorders and cancer, as well as explore outstanding questions about its function, regulation and potential use as a biomarker for anti-mitotic therapies.

    Keywords: p53, USP28, 53BP1, p21, c-Myc, neurodevelopment, Microcephaly, Apoptosis

    Received: 18 Jun 2024; Accepted: 06 Sep 2024.

    Copyright: © 2024 Stracker. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

    * Correspondence: Travis H. Stracker, Radiation Oncology Branch, Center for Cancer Research, National Cancer Institute (NIH), Bethesda, 20892, Maryland, United States

    Disclaimer: All claims expressed in this article are solely those of the authors and do not necessarily represent those of their affiliated organizations, or those of the publisher, the editors and the reviewers. Any product that may be evaluated in this article or claim that may be made by its manufacturer is not guaranteed or endorsed by the publisher.