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Tumor fibroblast-derived epiregulin promotes growth of colitis-associated neoplasms through ERK.

Clemens Neufert1, Christoph Becker, Özlem Türeci

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Epiregulin (EREG) drives the growth of colitis-associated tumors by promoting intestinal epithelial cell proliferation. Tumor-associated fibroblasts producing EREG significantly enhance tumor development, highlighting their crucial role in colitis-associated neoplasms.

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Area of Science:

  • Gastroenterology
  • Oncology
  • Molecular Biology

Background:

  • Colitis-associated cancers (CAC) lack well-defined molecular mechanisms.
  • Epiregulin (EREG) is differentially expressed in CAC models and patient cohorts.

Purpose of the Study:

  • To elucidate the role of EREG and tumor-associated fibroblasts in CAC development.
  • To investigate the molecular pathways linking EREG to tumor growth in colitis.

Main Methods:

  • Comparative whole-genome expression profiling in mouse models and human patient cohorts.
  • Functional studies using Ereg-deficient mice and adoptive transfer of fibroblasts.
  • Analysis of ERK activation in intestinal epithelial cells (IECs).

Main Results:

  • EREG expression is significantly upregulated in CAC, but not sporadic colorectal cancer.
  • Ereg-deficient mice are protected from CAC, indicating EREG promotes tumor growth, not initiation.
  • Fibroblast-derived EREG activates ERK signaling in IECs, driving proliferation and tumor development.
  • Adoptive transfer of EREG-producing fibroblasts augments CAC growth in vivo.

Conclusions:

  • EREG and tumor-associated fibroblasts are critical drivers of tumor growth in colitis-associated neoplasms.
  • Targeting EREG or EREG-producing fibroblasts may offer therapeutic strategies for CAC.