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Purification of Ubiquitinated p53 Proteins from Mammalian Cells
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Purification of Ubiquitinated p53 Proteins from Mammalian Cells

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The Role of JMY in p53 Regulation

Omanma Adighibe1, Francesco Pezzella2

  • 1Nuffield Division of Clinical Laboratory Science-Radcliffe Department of Medicine, University of Oxford, John Radcliffe Hospital, Oxford OX3 DU, UK. omanezi@gmail.com.

Cancers
|June 3, 2018
PubMed

Insights

Junctional Mediating and Regulating Y protein (JMY) influences tumor suppressor protein p53 activity following DNA damage, promoting apoptosis. JMY also enhances cell motility, suggesting dual roles in tumor suppression and metastasis.

Area of Science:

  • Molecular Biology
  • Cell Biology
  • Cancer Research

Background:

  • DNA damage triggers tumor suppressor protein p53 activation, leading to cell cycle arrest or apoptosis.
  • Junctional Mediating and Regulating Y protein (JMY) is a known regulator of p53.
  • The precise role of JMY in p53-mediated cellular responses requires further elucidation.

Purpose of the Study:

  • To investigate the role of JMY in p53-regulated apoptosis following DNA damage.
  • To explore the impact of JMY on cellular adhesion and motility.
  • To determine the dual capabilities of JMY in cancer progression.

Main Methods:

  • Western blotting to assess protein levels of JMY and p53.
  • Immunofluorescence to determine subcellular localization of JMY.
  • Co-immunoprecipitation assays to identify JMY-interacting proteins.
  • Quantitative real-time PCR to measure gene expression of adhesion molecules.
  • Cell migration and invasion assays.

Main Results:

  • DNA damage induces nuclear upregulation of JMY.
  • JMY forms a co-activator complex with p300/CREB-binding protein (p300/CBP), Apoptosis-stimulating protein of p53 (ASPP), and Stress responsive activator of p53 (Strap).
  • This complex enhances p53-mediated transcription of apoptosis-related genes, but not cell cycle arrest genes.
  • JMY downregulates Cadherin expression and promotes actin nucleation, increasing cell motility and metastasis.
  • JMY exhibits both tumor suppressive and metastasis-promoting functions.

Conclusions:

  • JMY directs p53 activity towards apoptosis following DNA damage.
  • JMY's regulation of cell adhesion and motility suggests a role in promoting tumor metastasis.
  • JMY possesses a dual function, acting as both a tumor suppressor and a promoter of metastasis.
Keywords:
JMYapoptosismotilityp53regulation

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