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Suppression of skin tumorigenesis in c-Jun NH(2)-terminal kinase-2-deficient mice

N Chen1, M Nomura, Q B She

  • 1The Hormel Institute, University of Minnesota, 801 16th Avenue NE, Austin, MN 55912, USA.

Cancer Research
|May 19, 2001
PubMed

Insights

The study reveals that JNK2 deficiency in mice significantly reduces tumor promotion caused by 12-O-tetradecanoylphorbol-13-acetate (TPA). This highlights JNK2

Area of Science:

  • Molecular Biology
  • Oncology
  • Signal Transduction

Background:

  • c-Jun NH(2)-terminal kinase (JNK) is a mitogen-activated protein kinase (MAPK) involved in cellular responses to stimuli.
  • The specific role of JNK in tumor promotion and carcinogenesis remains incompletely understood.

Purpose of the Study:

  • To investigate the role of JNK2 in mediating tumor promotion and carcinogenesis.
  • To determine the impact of JNK2 deficiency on chemically induced skin tumors.

Main Methods:

  • Comparison of tumor development in JNK2-deficient (Jnk2(-/-)) mice and wild-type mice following 12-O-tetradecanoylphorbol-13-acetate (TPA) treatment.
  • Assessment of papilloma multiplicity, growth, and vascularization.
  • Analysis of TPA-induced phosphorylation of extracellular signal-regulated kinases and activator protein-1 DNA binding activity.

Main Results:

  • JNK2-deficient mice exhibited significantly lower papilloma multiplicity compared to wild-type mice after TPA treatment.
  • Papillomas in wild-type mice showed more rapid growth and better vascularization than those in JNK2-deficient mice.
  • TPA-induced phosphorylation of extracellular signal-regulated kinases and activator protein-1 DNA binding activity were suppressed in JNK2-deficient mice.

Conclusions:

  • JNK2 plays a critical role in the tumor promotion process.
  • JNK2 signaling is essential for mediating the effects of TPA in skin carcinogenesis.

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