Related Experiment Video

Updated: Jun 23, 2026

Real-time Imaging of Myeloid Cells Dynamics in ApcMin/+ Intestinal Tumors by Spinning Disk Confocal Microscopy
05:21

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Published on: October 6, 2014

The Ron receptor tyrosine kinase is not required for adenoma formation in Apc(Min/+) mice

Sara E Meyer1, Susan E Waltz, Kathleen H Goss

  • 1Department of Cancer and Cell Biology, University of Cincinnati, Cincinnati, Ohio, USA.

Molecular Carcinogenesis
|May 20, 2009
PubMed

Insights

Ron receptor tyrosine kinase may play a role in normal intestinal homeostasis. However, its absence did not affect tumor growth in Apc-mutant mice, suggesting Ron is not required for adenoma formation.

Area of Science:

  • Oncology
  • Molecular Biology
  • Gastroenterology

Background:

  • The Ron receptor tyrosine kinase is frequently overexpressed in human colon cancers, correlating with tumor progression.
  • Loss of the adenomatous polyposis coli (APC) tumor suppressor is an early event in most colon tumors, leading to beta-catenin stabilization.

Purpose of the Study:

  • To investigate the role of Ron signaling in early-stage intestinal tumorigenesis.
  • To determine if Ron is necessary for the development and growth of Apc-mutant adenomas.

Main Methods:

  • Generation of Apc-mutant (Apc(Min/+)) mice with and without functional Ron signaling.
  • Comparison of tumor burden, crypt proliferation, tumor histology, and beta-catenin localization between groups.

Main Results:

  • Apc(Min/+) mice lacking Ron signaling exhibited a significantly higher tumor burden compared to Apc(Min/+) mice with wild-type Ron.
  • Increased intestinal crypt proliferation was observed in Apc(Min/+) Ron-deficient mice.
  • Loss of Ron did not alter tumor size, histological appearance, or beta-catenin localization in Apc(Min/+) adenomas.

Conclusions:

  • Ron signaling may be involved in maintaining normal intestinal tissue homeostasis.
  • Ron expression is not essential for the initiation or progression of adenomas in the Apc(Min/+) mouse model of intestinal tumorigenesis.

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