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DDIT3/CHOP and the sarcoma fusion oncoprotein FUS-DDIT3/TLS-CHOP bind cyclin-dependent kinase 2

Christoffer Bento1, Mattias K Andersson, Pierre Aman

  • 1Lundberg Laboratory for Cancer Research, Department of Pathology, University of Gothenburg, Gothenburg, Sweden. christoffer.bento@llcr.med.gu.se

BMC Cell Biology
|December 19, 2009
PubMed
Abstract

Insights

The DDIT3 gene, involved in cell cycle arrest and apoptosis, binds to CDK2. This interaction with CDK2 may explain many of DDIT3

Area of Science:

  • Molecular Biology
  • Cell Biology
  • Oncology

Background:

  • The DDIT3 gene encodes a transcription factor in the CCAAT/enhancer binding protein (C/EBP) family.
  • DDIT3 is activated by cellular stress, inducing G1 arrest and apoptosis.
  • DDIT3 forms a fusion oncogene, FUS-DDIT3, linked to myxoid/round-cell liposarcomas (MLS/RCLS).

Purpose of the Study:

  • To identify interaction partners of DDIT3 and the oncogenic FUS-DDIT3.
  • To investigate the role of G1 cyclins and cyclin-dependent kinases in DDIT3 function.

Main Methods:

  • Screening for interaction partners of DDIT3 and FUS-DDIT3.
  • Assessing binding affinities with G1 cyclins and cyclin-dependent kinases.
  • Analyzing CDK2 interactions with cytoskeletal proteins.

Main Results:

  • Both FUS-DDIT3 and normal DDIT3 were found to bind to CDK2.
  • Cells expressing FUS-DDIT3 and DDIT3 showed increased CDK2 affinity for cytoskeletal proteins.

Conclusions:

  • DDIT3 directly binds to CDK2.
  • The interaction between DDIT3 and CDK2 is a key mechanism underlying DDIT3's biological effects.

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