Related Experiment Video

Updated: Jun 12, 2026

Two- and Three-Dimensional Live Cell Imaging of DNA Damage Response Proteins
10:24

Two- and Three-Dimensional Live Cell Imaging of DNA Damage Response Proteins

Published on: September 28, 2012

JimMY on the stage: Linking DNA damage with cell adhesion and motility

Yingqun Wang1

  • 1Department of Cancer Biology, Abramson Family Cancer Research Institute, University of Pennsylvania, Philadelphia, PA, USA. yingqunw@mail.med.upenn.edu

Cell Adhesion & Migration
|June 25, 2010
PubMed

Insights

Cellular DNA damage triggers responses to maintain genome integrity. A study reveals JMY protein coordinates cell adhesion and motility with DNA damage response, suggesting it as a therapeutic target for cancer.

Area of Science:

  • Molecular Biology
  • Cell Biology
  • Cancer Research

Background:

  • Cells possess intricate DNA damage response (DDR) systems to maintain genome integrity against genotoxic stress.
  • Defects in DDR are linked to aging and cancer development.
  • Tumor suppressor p53 is crucial in DDR, mediating cell cycle arrest or apoptosis.

Discussion:

  • A novel p53-mediated cellular response involves modulating cell adhesion and motility.
  • The p53 co-factor JMY (Jumonji domain-containing protein) plays a multifunctional role.
  • JMY coordinates nuclear p53 activity with cellular adhesion and migration processes.

Key Insights:

  • JMY links the nuclear DNA damage response to the regulation of cell movement.
  • Aberrant JMY activity or localization may promote tumor invasion and metastasis.
  • JMY emerges as a potential therapeutic target for combating cancer progression.

Outlook:

  • Further research into JMY's role in DDR and cell motility is warranted.
  • Targeting JMY could offer new strategies for cancer therapy.
  • Understanding JMY's regulation may elucidate mechanisms of aging and cancer.

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