Reduced proliferation and cell adhesion in endometriosis

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Endometriotic lesions showed reduced cell proliferation and EGF expression but exhibited dedifferentiation with decreased E-cadherin complex expression, suggesting invasive properties.

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Abstract

Endometriosis is defined as endometriotic tissues growing outside the uterine cavity. The cell biological processes responsible for the pathogenesis of this disease are not well understood. In order to detect differences in proliferative activity between endometria and endometriotic lesions, Ki67 staining was analysed. In addition, expression of epidermal growth factor (EGF) and its receptor was examined using immunohistochemistry. For dedifferentiation processes pointing to invasive properties of the uterine epithelium, the presence of the adhesion complex E-cadherin with the associated alpha- and beta-catenin was investigated. Specimens of endometrium in the proliferative phase of 36 patients without, and 79 patients with, endometriosis together with endometriotic lesions were studied. The study revealed a significantly reduced proliferation activity in uterine epithelium within the ectopic lesions but no differences between eutopic endometria of non-affected and affected patients. Furthermore, a lower expression of both EGF and its receptor in the epithelial cells of the ectopic glands was observed. The adhesion complex E-cadherin, together with alpha-, and beta-catenin, was slightly reduced in uterine epithelial cells of women with endometriosis and less expressed in endometriotic lesions. The results indicate that epithelial cells of endometriotic lesions are not hyperproliferative, but do appear to dedifferentiate, displaying an invasive character.

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Condition tags

endometriosis

MeSH descriptors

Endometriosis Adult Cell Adhesion Cell Adhesion Cell Division Cell Division Endometriosis Endometriosis Epidermal Growth Factor Epidermal Growth Factor ErbB Receptors ErbB Receptors Female Humans Immunohistochemistry Ki-67 Antigen Ki-67 Antigen

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europepmc
last seen: 2026-06-20T06:14:18.781669+00:00
openalex
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