Tumor suppressive role for kinases phosphorylating p53 in DNA damage-induced apoptosis

Satomi Yogosawa1, Kiyotsugu Yoshida1

  • 1Department of Biochemistry, Jikei University School of Medicine, Tokyo, Japan.

Cancer Science
|September 8, 2018
PubMed

Insights

Tumor suppressor p53 protein levels rise under stress, triggering apoptosis to prevent cancer. This review explores p53 phosphorylation by kinases and its role in cancer therapy.

Area of Science:

  • Molecular biology
  • Cancer research
  • Cellular signaling

Background:

  • The tumor suppressor p53 is crucial for cancer prevention.
  • p53 is activated by cellular stress, initiating DNA repair, cell-cycle arrest, senescence, and apoptosis.
  • Post-translational modifications, especially phosphorylation, regulate p53 activity and gene expression.

Purpose of the Study:

  • To review the roles of p53 phosphorylation and its kinases in inducing apoptosis.
  • To discuss the relationship between p53 phosphorylation, its kinases, and kinase control mechanisms.
  • To explore novel therapeutic strategies targeting p53 phosphorylation in various cancers.

Main Methods:

  • Literature review of existing studies on p53 phosphorylation and kinases.
  • Analysis of molecular mechanisms underlying p53-mediated apoptosis.
  • Synthesis of information on therapeutic approaches targeting the p53 pathway.

Main Results:

  • p53 phosphorylation is a critical regulator of apoptosis induction in cancer cells.
  • Specific serine/threonine kinases modulate p53 phosphorylation and downstream gene expression.
  • Understanding kinase activity control is essential for p53-mediated cancer prevention.

Conclusions:

  • p53 phosphorylation and its associated kinases are vital for apoptosis and cancer prevention.
  • Further investigation into kinase regulation is needed.
  • Targeting p53 phosphorylation offers a promising therapeutic avenue for diverse cancers.

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