c-Jun induces apoptosis of starved BM2 monoblasts by activating cyclin A-CDK2

Biochem Biophys Res Commun. 2007 Feb 2;353(1):92-7. doi: 10.1016/j.bbrc.2006.11.124. Epub 2006 Dec 4.

Abstract

c-Jun is one of the major components of the activating protein-1 (AP-1), the transcription factor that participates in regulation of proliferation, differentiation, and apoptosis. In this study, we explored functional interactions of the c-Jun protein with several regulators of the G1/S transition in serum-deprived v-myb-transformed chicken monoblasts BM2. We show that the c-Jun protein induces expression of cyclin A, thus up-regulating activity of cyclin A-associated cyclin-dependent kinase 2 (CDK2), and causing massive programmed cell death of starved BM2cJUN cells. Specific inhibition of CDK2 suppresses frequency of apoptosis of BM2cJUN cells. We conclude that up-regulation of cyclin A expression and CDK2 activity can represent important link between the c-Jun protein, cell cycle machinery, and programmed cell death pathway in leukemic cells.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Apoptosis*
  • Cell Line
  • Cell Transformation, Neoplastic / metabolism*
  • Chickens
  • Culture Media, Serum-Free
  • Cyclin-Dependent Kinase 2 / metabolism*
  • Enzyme Activation
  • Leukemia, Monocytic, Acute / metabolism*
  • Oxidative Stress*
  • Proto-Oncogene Proteins c-jun / metabolism*
  • Signal Transduction

Substances

  • Culture Media, Serum-Free
  • Proto-Oncogene Proteins c-jun
  • Cyclin-Dependent Kinase 2