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RESEARCH ARTICLE The Cytoskeletal Proteins a-actinin, Ezrin, and Talin are De-expressed in Endometriosis and Endometrioid Carcinoma Compared With Normal Uterine Epithelium Michael Slater, PhD,* M. Cooper, MBBS, FRACOG,*w and C. R. Murphy, DSc* cytoskeletal protein that bundles actin microfilaments and Abstract: In this retrospective study on banked tissue, we found links these filaments directly to integrin-adhesion recep- that a-actinin and talin were completely de-expressed in both tors. Phosphoinositides bind to a-actinin, regulating its endometriosis and endometrioid carcinoma tissue. Some patchy, localization. Alpha-actinin participates in the rapid depolarized labeling for ezrin was noted in the endometrioid organization of actin into microspikes at the cell-cell carcinoma but not in endometriosis. The loss of these proteins in junctions and leads to active cell separation. The actin- both endometriosis and endometrioid carcinoma tissue indicates binding proteins a-actinin, tropomyosin, gelsolin, and a significant change in the integrity of these tissues compared vinculinin are present in uterine epithelial cells. with normal and the possibility that individual cells may break Ezrin, a membrane cytoskeleton linker, is involved away from the parent histology due to loss of cell adhesion. in cellular functions, including epithelial cell migration, It also indicates a similarity between endometrioid cancer and morphogenesis, formation
Applied Immunohistochemistry & Molecular Morphology – Wolters Kluwer Health
Published: Jun 1, 2007
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