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Ninjurin 2, a Cell Adhesion Molecule and a Target of p53, Modulates Wild-Type p53 in Growth Suppression and Mutant

Jin Zhang1, Xiangmudong Kong1, Hee Jung Yang1

  • 1Comparative Oncology Laboratory, The University of California, Davis, CA 95616, USA.

Cancers
|January 11, 2024
PubMed

Insights

Nerve injury-induced protein 2 (NINJ2) interacts with p53, forming a feedback loop. This NINJ2-p53 loop suppresses growth with wild-type p53 but promotes it with mutant p53.

Area of Science:

  • Molecular biology
  • Cell biology
  • Cancer research

Background:

  • Nerve injury-induced protein 1 (NINJ1) and NINJ2 are homophilic adhesion molecules involved in nerve regeneration.
  • The NINJ1-p53 interaction is crucial for tumor suppression.
  • The biological role of NINJ2 remains largely unexplored.

Purpose of the Study:

  • To investigate the role of NINJ2 in DNA damage response and its relationship with p53.
  • To elucidate the functional impact of the NINJ2-p53 interaction in cancer cells.

Main Methods:

  • Utilized in vitro cell lines and genetically engineered mouse embryo fibroblasts (MEFs).
  • Assessed NINJ2 induction by DNA damage.
  • Examined the effect of NINJ2 loss on p53 expression and cell phenotypes.
  • Investigated NINJ2's role in both wild-type and mutant p53 contexts.

Main Results:

  • NINJ2 is induced by DNA damage in a p53-dependent manner.
  • Loss of NINJ2 enhances wild-type p53 expression, leading to growth suppression and senescence.
  • NINJ2 regulates mutant p53, and its loss promotes cell growth and migration in mutant p53-expressing cells.

Conclusions:

  • NINJ2 and p53 form a mutual regulatory negative feedback loop.
  • The NINJ2-p53 loop exhibits opposing functions: growth suppression in wild-type p53 and growth promotion in mutant p53.
Keywords:
NINJ2cell proliferationcellular senescencep53

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