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HIPK2 is involved in cell proliferation and its suppression promotes growth arrest independently of DNA damage

S Iacovelli1, L Ciuffini, C Lazzari

  • 1Department of Experimental Oncology, Regina Elena Cancer Institute, Rome, Italy.

Cell Proliferation
|May 15, 2009
PubMed
Abstract

Insights

Homeodomain-interacting protein kinase 2 (HIPK2) regulates cell-cycle arrest via p21(Waf-1/Cip-1) induction, independent of DNA damage. This study found HIPK2

Area of Science:

  • Molecular Biology
  • Cell Biology
  • Biochemistry

Background:

  • Homeodomain-interacting protein kinase 2 (HIPK2) is a serine/threonine kinase.
  • HIPK2 acts as a co-regulator for transcription factors in DNA damage response and development.
  • HIPK2 was initially identified as an interactor of the p53 oncosuppressor.

Purpose of the Study:

  • To investigate the potential cooperation between HIPK2 and p53 in cell differentiation.
  • To elucidate the role of HIPK2 in cell-cycle regulation and its dependence on DNA damage.

Main Methods:

  • Yeast two-hybrid screening using p53 as bait.
  • Measurement of HIPK2 expression and activity during skeletal muscle and hematopoietic differentiation.
  • HIPK2 depletion experiments to assess its effect on cell-cycle progression.

Main Results:

  • HIPK2 and p53 exhibited inverse expression patterns during skeletal muscle and hematopoietic differentiation, suggesting no cooperative activity in these processes.
  • HIPK2 depletion led to cell-cycle arrest.
  • This cell-cycle arrest was mediated by the induction of the cyclin-dependent kinase inhibitor p21(Waf-1/Cip-1).
  • HIPK2 activity was observed in cell-cycle-arresting conditions, including terminal differentiation and growth factor deprivation, and was independent of DNA damage.

Conclusions:

  • HIPK2 plays a role in cell-cycle regulation.
  • HIPK2-mediated cell-cycle regulation is dependent on p21(Waf-1/Cip-1).
  • HIPK2's function in cell-cycle regulation is independent of DNA damage.

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