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The p53-targeting human phosphatase hCdc14A interacts with the Cdk1/cyclin B complex and is differentially expressed

Michelle T Paulsen1, Adrienne M Starks, Frederick A Derheimer

  • 1Department of Radiation Oncology, Division of Radiation & Cancer Biology, University of Michigan Comprehensive Cancer Center, University of Michigan, Ann Arbor, MI 48109, USA. tenbroek@umich.edu

Molecular Cancer
|June 21, 2006
PubMed
Abstract

Insights

Human Cdc14A phosphatase (hCdc14A) is differentially expressed in cancers and interacts with p53. Its dysregulation may contribute to cancer development, with low expression linked to wild-type p53.

Area of Science:

  • Cell Biology
  • Molecular Biology
  • Cancer Research

Background:

  • hCdc14A, a cyclin-dependent kinase phosphatase, is involved in mitotic exit and centrosome duplication.
  • hCdc14A interacts with tumor suppressor p53, specifically dephosphorylating p53 at serine 315.
  • This study investigates hCdc14A expression and regulation in human tissues and cancer cells.

Purpose of the Study:

  • To develop antibodies against hCdc14A for expression analysis.
  • To investigate the differential expression of hCdc14A in human tissues and cancer cell lines.
  • To explore the regulation of hCdc14A expression by various inhibitors and its relationship with p53.

Main Methods:

  • Development of specific antibodies against hCdc14A.
  • Analysis of hCdc14A expression in human tissues and 75 cancer cell lines.
  • Treatment of cell lines with TSA, 5-aza-2'-deoxycytodine, and MG132 to assess hCdc14A induction.
  • Investigation of hCdc14A interaction with p53 and Cdk1/cyclin B complex.

Main Results:

  • hCdc14A exhibits differential expression across human tissues and cancer cell lines.
  • Expression of hCdc14A was significantly induced by TSA, 5-aza-2'-deoxycytodine, and MG132 in low-expressing cells.
  • Low hCdc14A expression showed a strong bias in cancer cell lines with wild-type p53.
  • Evidence suggests hCdc14A dephosphorylates p53 at serine 315 in vivo and forms a complex with Cdk1/cyclin B during interphase.

Conclusions:

  • hCdc14A is differentially expressed in human cancer cells.
  • hCdc14A interacts with both p53 and the Cdk1/cyclin B complex.
  • Dysregulation of hCdc14A expression may contribute to carcinogenesis.

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