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非恶性上皮细胞在人类子宫内膜异位症中可能具有侵袭性,缺乏肿瘤抑制分子E-钙黏蛋白。

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

作者信息

Gaetje R, Kotzian S, Herrmann G, Baumann R, Starzinski-Powitz A

机构信息

Humangenetik für Biologen der Universität, Universitaetsklinikum, Frankfurt am Main, Germany.

出版信息

Am J Pathol. 1997 Feb;150(2):461-7.

PMID:9033262
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC1858282/
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.

摘要

子宫内膜异位症是妇科最常见的疾病之一。它是一种组织学定义的非恶性疾病,其中在子宫外(例如腹膜、肠道或肺部)发现类似子宫内膜的组织。子宫内膜异位症的发病机制尚不清楚,但侵袭机制与该疾病的发展有关。事实上,在体外胶原侵袭试验中,来自人类子宫内膜异位活检组织的原代细胞具有侵袭性,而来自人类子宫内膜活检组织的原代细胞则没有。在这项研究中,发现这些体外具有侵袭性的子宫内膜异位细胞是缺乏E-钙黏蛋白的非恶性上皮细胞,E-钙黏蛋白在癌症中作为一种侵袭抑制分子发挥作用。免疫细胞化学显示,与正常子宫内膜切片相比,子宫内膜异位症组织切片中E-钙黏蛋白阴性上皮细胞类型增加。基于这些数据,我们提出在体外观察到的E-钙黏蛋白阴性侵袭性子宫内膜异位细胞代表迁移到异位(子宫外)部位并因此在体内导致子宫内膜异位症的细胞群体。因此,推测E-钙黏蛋白表达的丧失是子宫内膜异位症发病机制中的一个关键机制。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0d39/1858282/6b29734a824c/amjpathol00026-0082-b.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0d39/1858282/e986a987a612/amjpathol00026-0080-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0d39/1858282/810aa818f529/amjpathol00026-0081-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0d39/1858282/a8f5c9663d36/amjpathol00026-0082-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0d39/1858282/6b29734a824c/amjpathol00026-0082-b.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0d39/1858282/e986a987a612/amjpathol00026-0080-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0d39/1858282/810aa818f529/amjpathol00026-0081-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0d39/1858282/a8f5c9663d36/amjpathol00026-0082-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0d39/1858282/6b29734a824c/amjpathol00026-0082-b.jpg

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