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(American Journal of Pathology. 2000;156:671-683.)
© 2000 American Society for Investigative Pathology

Regular Articles

Site-Specific Epithelial-Mesenchymal Interactions in Digestive Neuroendocrine Tumors

An Experimental in Vivo and inVitro Study

Jérôme Dumortier*{dagger}, Christelle Ratineau*, Jean-Yves Scoazec*{ddagger}, Céline Pourreyron*§, Wena Anderson*§, Marie-France Jacquier*, Martine Blanc*, Christine Bernard*, Claire Bellaton*§, Lionel Remy*, Jean-Alain Chayvialle*{dagger} and Colette Roche*

From the Institut National de la Santé et de la Recherche Médicale, Unité-45,*
Fédération des Spécialités Digestives,{dagger}
Laboratoire Central d’Anatomie et de Cytologie Pathologiques,{ddagger}
and Ecole Pratique des Hautes Etudes,§
Hôpital Edouard Herriot, Lyon, France

Little is known about the functional interactions between digestive neuroendocrine tumor cells and their stromal microenvironment. The focus of our study is whether mesenchymal cells modulate peptide expression, cell proliferation, and invasiveness in digestive neuroendocrine tumor cells. We designed an experimental in vivo and in vitro study using the mouse enteroendocrine cell line STC-1. In vivo, STC-1 cells were injected subcutaneously in 18 immunosuppressed newborn rats. At day 21, all animals presented poorly differentiated neuroendocrine tumors with lung metastases. Subcutaneous tumors were usually limited by a capsule containing basement membrane components and myofibroblasts that presented a low mitotic index. Lung tumors were devoid of capsule and poor in myofibroblasts, and their mitotic index was high. The profile of peptide expression in STC-1 tumors was different from that of cultured STC-1 cells. In vitro, STC-1 cells were cultured with fibroblasts of different origins, including dermis, lung, digestive tract, and liver. Based on their origin, myofibroblasts differentially modulated hormone synthesis, proliferation, spreading, and adhesion of STC-1 cells. In conclusion, our results show that site-specific functional interactions between mesenchymal and neuroendocrine cells may contribute to modulating the behavior of digestive neuroendocrine tumors, depending on their growth site.




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