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In vivo activation of mitogen-activated protein kinases in rat intestinal neoplasia

L L Licato1, T O Keku, J I Wurzelmann

  • 1Department of Microbiology and Immunology, University of North Carolina at Chapel Hill 27599, USA.

Gastroenterology
|November 14, 1997
PubMed
Abstract

Insights

Mitogen-activated protein kinase (MAPK) cascades, specifically c-Jun N-terminal kinase (JNK) and extracellular signal regulating kinase (ERK), are highly activated during colorectal carcinoma progression. This activation is linked to the tumorigenic state, not just proliferation.

Area of Science:

  • Molecular Biology
  • Oncology
  • Cell Signaling

Background:

  • Colon cancer progression involves complex signaling pathways.
  • Mitogen-activated protein kinase (MAPK) cascades are implicated in cellular processes.
  • Investigating specific MAPK pathways like JNK and ERK in tumorigenesis is crucial.

Purpose of the Study:

  • To determine the role of c-Jun N-terminal kinase (JNK) and extracellular signal regulating kinase (ERK) activity in colon cancer progression.
  • To examine MAPK cascade activation during colonic tumorigenesis.

Main Methods:

  • Utilized the 1,2-dimethylhydrazine (DMH)-induced colon carcinoma rat model.
  • Assayed JNK and ERK activity in normal mucosa and DMH-induced tumors using in vitro kinase assays.
  • Analyzed K-ras gene mutations in colonic tumors.

Main Results:

  • JNK and ERK activity showed minimal change in hyperproliferative mucosa but increased significantly (23-fold and 29-fold, respectively) in colonic neoplasms.
  • Activating protein-1 binding was strongly induced in tumors.
  • MAPK activation did not correlate with K-ras mutations.

Conclusions:

  • Both JNK and ERK MAPKs are significantly activated in late-stage colorectal carcinoma.
  • MAPK activation is associated with the tumorigenic state of colorectal cancer.
  • These findings highlight the role of specific MAPK pathways in colorectal cancer progression.

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