The contribution of neuronal-glial-endothelial-epithelial interactions to colon carcinogenesis

Cell Mol Life Sci. 2014 Sep;71(17):3191-7. doi: 10.1007/s00018-014-1642-z. Epub 2014 May 22.

Abstract

Several different cell types constitute the intestinal wall and interact in different manners to maintain tissue homeostasis. Elegant reports have explored these physiological cellular interactions revealing that glial cells and neurons not only modulate peristalsis and mechanical stimulus in the intestines but also control epithelial proliferation and sub-epithelial angiogenesis. Although colon carcinoma arises from epithelial cells, different sub-epithelial cell phenotypes are known to support the manifestation and development of tumors from their early steps on. Therefore, new perspectives in cancer research have been proposed, in which neurons and glial cells not only lead to higher cancer cell proliferation at the tumor invasion front but also further enhance angiogenesis and neurogenesis in tumors. Transformation of physiological neural activity into a pro-cancer event is thus discussed for colon carcinogenesis herein.

Publication types

  • Review

MeSH terms

  • Adenocarcinoma / etiology
  • Adenocarcinoma / pathology*
  • Adenoma / etiology
  • Adenoma / pathology
  • Animals
  • Cell Communication
  • Cell Transformation, Neoplastic / genetics
  • Cell Transformation, Neoplastic / pathology*
  • Colonic Neoplasms / etiology
  • Colonic Neoplasms / pathology*
  • Disease Progression
  • Endothelial Cells / physiology*
  • Enteric Nervous System / pathology
  • Epithelial Cells / physiology*
  • Feedback, Physiological
  • Humans
  • Inflammation
  • Intestinal Mucosa / pathology
  • Intestines / blood supply
  • Mice
  • Mice, Transgenic
  • Mutation
  • Neoplasm Invasiveness
  • Neoplastic Stem Cells / physiology
  • Neovascularization, Pathologic / physiopathology
  • Neuroglia / physiology*
  • Neurons / physiology*
  • Serotonin / physiology
  • Tumor Microenvironment

Substances

  • Serotonin