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Published on: August 4, 2019

Cyclin K as a direct transcriptional target of the p53 tumor suppressor

Toshiki Mori1, Yoshio Anazawa, Kuniko Matsui

  • 1Human Genome Center, Institute of Medical Science, University of Tokyo, 4-6-1 Shirokanedai, Minato-ku, Tokyo 108-8639, Japan.

Neoplasia (New York, N.Y.)
|May 4, 2002
PubMed

Insights

Cyclin K, a transcription regulator, is upregulated by p53 in glioblastoma cells. Overexpression of cyclin K inhibits cancer cell growth, suggesting a role in cell cycle or apoptosis.

Area of Science:

  • Molecular Biology
  • Cancer Research
  • Cell Cycle Regulation

Background:

  • Cyclin K is a novel "transcription" cyclin.
  • It may regulate both CDK and transcription.
  • Its role in cancer, particularly glioblastoma, is largely unknown.

Purpose of the Study:

  • To investigate the regulation of cyclin K by p53.
  • To determine the functional impact of cyclin K on cancer cell proliferation.

Main Methods:

  • cDNA microarray analysis to assess cyclin K mRNA levels.
  • Electrophoretic mobility-shift assay (EMSA) to study p53-DNA binding.
  • Heterologous reporter assays to evaluate transcriptional activity.
  • Colony-formation assays to assess cell growth suppression.

Main Results:

  • Cyclin K mRNA expression was significantly increased in p53-deficient glioblastoma cells upon p53 introduction.
  • A specific p53-binding site (p53BS) in intron 1 of the cyclin K gene was identified and shown to bind p53 protein.
  • The p53BS demonstrated p53-dependent transcriptional activity.
  • Overexpression of cyclin K led to suppressed growth in multiple cancer cell lines (T98G, U373MG, SW480).

Conclusions:

  • p53 directly regulates cyclin K transcription via a specific binding site.
  • Cyclin K may function as a tumor suppressor by inhibiting cancer cell proliferation.
  • Cyclin K is implicated in p53-mediated regulation of cell cycle or apoptosis.

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