Nonmalignant epithelial cells, potentially invasive in human endometriosis, lack the tumor suppressor molecule E-cadherin.

R Gaetje, S Kotzian, G Herrmann, R Baumann, R Baümann, Anna Starzinski‐Powitz, A Starzinski-Powitz
The American journal of pathology · 1997 · vol. 150(2) , pp. 461–7 · PMID:9033262 · W129298122
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Invasive endometriotic epithelial cells, potentially causing endometriosis, were found to lack the invasion suppressor molecule E-cadherin, unlike normal endometrial cells.

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Abstract

Endometriosis is one of the most frequent diseases in gynecology. It is a histologically defined nonmalignant disease in which endometrium-like tissue is found outside the uterus (for example, peritoneum, gut, or lung). The pathogenesis of endometriosis is unknown, but invasive mechanisms have been implicated in the development of the disease. Indeed, primary cells from human endometriotic biopsies but not from human endometrial biopsies are invasive in an in vitro collagen invasion assay. In this study, these in vitro invasive endometriotic cells were found to be nonmalignant epithelial cells lacking E-cadherin, which acts as an invasion suppressor molecule in carcinomas. Immunocytochemistry showed that the E-cadherin-negative epithelial cell type was increased in sections of endometriosis tissue as compared with sections of eutopic endometrium. On the basis of these data we propose that the E-cadherin-negative invasive endometriotic cells seen in vitro represent the cell population that migrates to ectopic (extrauterine) locations and thus causes endometriosis in vivo. Accordingly, the loss of E-cadherin expression is postulated to constitute a crucial mechanism in the pathogenesis of endometriosis.

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Condition tags

mesh:D004715endometriosis

MeSH descriptors

Cadherins Endometriosis Endometriosis Endometrium Endometrium Cadherins Cell Movement Cells, Cultured Collagen Endometriosis Endometrium Epithelium Epithelium Epithelium Female Gels Humans Immunohistochemistry

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