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Physical interaction of p73 with c-Myc and MM1, a c-Myc-binding protein, and modulation of the p73 function

Ken-ichi Watanabe1, Toshinori Ozaki, Takahito Nakagawa

  • 1Division of Biochemistry, Chiba Cancer Center Research Institute, Chiba 260-8717, Japan.

The Journal of Biological Chemistry
|February 15, 2002
PubMed

Insights

The protein MM1 interacts with p73 alpha, enhancing its tumor-suppressing activity by preventing inhibition from c-Myc. This discovery offers new insights into p73 regulation and cancer research.

Area of Science:

  • Molecular Biology
  • Cancer Research
  • Protein Interactions

Background:

  • The tumor suppressor p73, homologous to p53, regulates cell cycle arrest and apoptosis through transactivation.
  • The unique COOH-terminal region of p73 modulates its DNA-binding and transactivation functions.
  • Understanding proteins interacting with p73 is crucial for elucidating its regulatory mechanisms.

Purpose of the Study:

  • To identify and characterize cellular proteins interacting with the COOH-terminal region of p73 alpha.
  • To investigate the regulatory role of these interacting proteins on p73 alpha activity.
  • To explore the functional consequences of these interactions in cellular processes.

Main Methods:

  • Yeast-based two-hybrid screening using a human fetal brain cDNA library.
  • In vitro pull-down assays and co-immunoprecipitation in mammalian cells.
  • Reporter gene assays to assess transcriptional activity on p53/p73-responsive promoters (Bax, PG13, p21(waf1)).

Main Results:

  • MM1, a nuclear c-Myc-binding protein, was identified as a p73 alpha interacting partner.
  • MM1 specifically co-immunoprecipitated with p73 alpha, but not p73 beta or p53.
  • MM1 enhanced p73 alpha-dependent transcription and growth suppression in p53-deficient cells.
  • c-Myc inhibited p73 alpha transcriptional activity, an effect reduced by MM1 expression.

Conclusions:

  • MM1 acts as a molecular partner for p73 alpha, specifically counteracting c-Myc-mediated inhibition.
  • This interaction modulates p73 alpha's transcriptional activity and growth-suppressive functions.
  • MM1 represents a potential target for therapeutic strategies involving p73 in cancer.

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