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The platelet-derived growth factor controls c-myc expression through a JNK- and AP-1-dependent signaling pathway

Carlo Iavarone1, Annunziata Catania, Maria Julia Marinissen

  • 1Dipartimento di Biologia e Patologia Cellulare e Molecolare, Università degli Studi di Napoli Federico II, 80131 Napoli, Italy.

The Journal of Biological Chemistry
|October 3, 2003
PubMed

Insights

The JNK-Jun pathway regulates cell processes. This study reveals JNK activation is crucial for platelet-derived growth factor (PDGF)-induced c-myc expression, identifying a new link between tyrosine kinases and cell growth/death.

Area of Science:

  • Molecular Biology
  • Cell Signaling
  • Oncogenesis

Background:

  • The c-Jun N-terminal kinase (JNK) pathway, activated by various stimuli, phosphorylates AP-1 transcription factors, influencing cell growth, differentiation, and apoptosis.
  • Despite its importance, specific targets of the JNK-Jun pathway remain largely unidentified, limiting understanding of its downstream effects.

Purpose of the Study:

  • To investigate the role of JNK in regulating c-myc proto-oncogene expression.
  • To identify specific AP-1 binding elements involved in PDGF-mediated c-myc transactivation.

Main Methods:

  • Investigated JNK's requirement for PDGF-induced c-myc expression.
  • Identified and characterized an AP-1-responsive element in the c-myc promoter.
  • Assessed in vivo recruitment of c-Jun and JunD to the c-myc promoter.

Main Results:

  • JNK activation is essential for platelet-derived growth factor (PDGF)-induced c-myc expression.
  • A conserved AP-1-responsive element in the c-myc promoter binds c-Jun and JunD.
  • This element mediates PDGF-dependent transactivation of the c-myc promoter.

Conclusions:

  • A novel pathway links tyrosine kinase receptors (like PDGF) to c-myc expression via JNK-mediated AP-1 activation.
  • This mechanism provides insight into how JNK and Jun proteins regulate cell proliferation and apoptosis through c-myc.
  • The findings highlight a new regulatory axis impacting proto-oncogene expression and cellular fate.

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