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

Travis H Stracker1

  • 1Center for Cancer Research, Radiation Oncology Branch, National Cancer Institute, Bethesda, MD, United States.

Frontiers in Cell and Developmental Biology
|October 14, 2024
PubMed

Insights

A new pathway, the mitotic surveillance pathway, activates the tumor suppressor p53 (encoded by TP53) in response to cell division delays, promoting genomic stability and influencing development and disease.

Area of Science:

  • Molecular Biology
  • Cell Biology
  • Genetics

Background:

  • The transcription factor p53 (TP53) is crucial for tumor suppression and influences mammalian development.
  • p53 signaling mediates cell fate decisions under various stress conditions.
  • Mitotic progression is critical for genomic stability.

Purpose of the Study:

  • To review the identification and function of the newly discovered mitotic surveillance pathway.
  • To discuss the roles of USP28 and 53BP1 in p53 activation during mitotic delays.
  • To explore the implications of this pathway in neurodevelopmental disorders, cancer, and anti-mitotic therapies.

Main Methods:

  • Literature review of recent findings on the mitotic surveillance pathway.
  • Analysis of the roles of USP28 and 53BP1 in p53 activation.
  • Discussion of potential clinical applications and future research directions.

Main Results:

  • A novel pathway, termed mitotic surveillance or mitotic stopwatch, activates p53 in response to delayed mitosis.
  • USP28 and 53BP1 are key proteins in this pathway, controlling cell fate and genomic stability.
  • This pathway offers new insights into development, cancer, and therapeutic strategies.

Conclusions:

  • The mitotic surveillance pathway represents a significant advancement in understanding p53 regulation.
  • Further research is needed to fully elucidate its function, regulation, and therapeutic potential.
  • USP28, 53BP1, and p53 interactions are critical for maintaining genomic integrity.
Keywords:
53BP1USP28apoptosisc-MYCcancermicrocephalyneurodevelopmentp53

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