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(American Journal of Pathology. 2000;157:1863-1874.)
© 2000 American Society for Investigative Pathology

Regular Articles

Modulation of Human Colon Tumor-Stromal Interactions by the Endothelin System

Giorgia Egidy*, Lucienne Juillerat-Jeanneret{dagger}, Jean-François Jeannin{ddagger}, Petra Korth*, Fred T. Bosman{dagger} and Florence Pinet*

From INSERM Unit 36,*
College of France, Paris, France; the Institute of Pathology,{dagger}
Lausanne, Switzerland; and Faculty of Medicine,{ddagger}
INSERM U517/Ecole Pratique des Hautes Etudes, Dijon, France

Tumor neovascularization is considered to be a critical step in the development of a malignant tumor. Endothelin (ET)-1 is a powerful vasoconstrictor and mitogenic peptide that is produced by many cancer cell lines. The cellular distribution of the ET components was evaluated in human colon tumors and compared to normal colon. There was more of the ET components (preproET-1, endothelin-converting enzyme-1, and ETA and ETB receptors) in adenomas and adenocarcinomas than in the normal colon. There was overproduction of preproET-1 and endothelin-converting enzyme-1 in carcinoma cells and stromal vessels, suggesting that they are a local source of ET-1. ETA receptors were present in stromal myofibroblasts of neoplastic tissue, and there were large amounts of ETB receptors in the endothelium and myofibroblasts. There was also a redistribution of {alpha}-smooth muscle actin-positive cells in the vascular structures of tumors. An experimental rat model of induced colon cancer treated for 30 days with bosentan, a mixed antagonist of both ET receptors, confirmed the morphological changes observed during the tumor vascularization. Our data suggest that ET-1 and its receptor play a role in colon cancer progression, with ET-1 functioning as a negative modulator of the stromal response.




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