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Suppression of Ras-stimulated transformation by the JNK signal transduction pathway

Norman J Kennedy1, Hayla K Sluss, Stephen N Jones

  • 1Howard Hughes Medical Institute, University of Massachusetts Medical School, Worcester, Massachusetts 01605, USA.

Genes & Development
|March 12, 2003
PubMed

Insights

The c-Jun NH(2)-terminal kinase (JNK) pathway, while involved in cell transformation, appears to suppress tumor growth in vivo. JNK deficiency unexpectedly increased tumor development, suggesting a tumor-suppressive role.

Area of Science:

  • Molecular biology
  • Oncology
  • Cell signaling

Background:

  • The c-Jun NH(2)-terminal kinase (JNK) pathway regulates the activator protein-1 (AP-1) transcription factors.
  • JNK signaling is implicated in oncogenic transformation and cancer development.

Purpose of the Study:

  • To investigate the role of JNK in Ras-stimulated cellular transformation and tumor development.
  • To determine if JNK is essential for in vivo tumor formation.

Main Methods:

  • Studied JNK-deficient cells in Ras-stimulated transformation assays.
  • Assessed tumor development in vivo using JNK-deficient models.
  • Performed complementation assays to confirm the observed phenotype.

Main Results:

  • JNK plays a role in in vitro transformation but is not required for tumor development.
  • JNK deficiency led to a significant increase in tumor nodule number and growth in vivo.
  • Complementation assays confirmed that JNK deficiency caused the enhanced tumor development phenotype.

Conclusions:

  • Contrary to expectations, JNK's normal function may be to suppress tumor development in vivo.
  • Loss-of-function mutations in the JNK pathway observed in human tumors support its potential tumor-suppressive role.

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