RNAi-mediated blocking of ezrin reduces migration of ectopic endometrial cells in endometriosis

Ezrin is a member of the ezrin-radixin-moesin (ERM) family of membrane-cytoskeletal linkage proteins. It is important for maintenance of cell shape, adhesion, migration and division. The overexpression of ezrin in some tumours is associated with increased cell migration that is mediated by the Rho/R...

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Published inMolecular human reproduction Vol. 18; no. 9-10; pp. 435 - 441
Main Authors JIANG, Qiao-Ying, XIA, Jian-Mei, DING, Hai-Gang, FEI, Xiang-Wei, JUN LIN, WU, Rui-Jin
Format Journal Article
LanguageEnglish
Published Oxford Oxford University Press 01.09.2012
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Summary:Ezrin is a member of the ezrin-radixin-moesin (ERM) family of membrane-cytoskeletal linkage proteins. It is important for maintenance of cell shape, adhesion, migration and division. The overexpression of ezrin in some tumours is associated with increased cell migration that is mediated by the Rho/ROCK family of small GTPases. To investigate the role of ezrin in the migration of ectopic endometrial cells in endometriosis, we conducted real-time quantitative RT-PCR analysis of the eutopic and ectopic endometrium from women with endometriosis compared with those without the disease. RNAi, wound healing assays and western blot analysis of endometriotic cells were also included in this research. We found significantly higher levels of mRNA expression of ezrin (0.42 versus 0.27, P < 0.05), RhoA (0.99 versus 0.74, P < 0.05), RhoC (0.79 versus 0.43, P < 0.005) and ROCK1 (0.68 versus 0.38, P < 0.005) in the ectopic endometrial cells compared with the eutopic endometrial cells in endometriosis. Blocking ezrin with small-interfering RNA reduced the migration of ectopic endometrial cells with decreased expression of RhoA (42.68%), RhoC (58.42%) and ROCK1 (59.88%). Our results indicate that the over-expression of ezrin in endometriosis may play a significant role in the migration of endometrial cells of endometriosis, and the RhoC/Rock pathway may provide a promising treatment target.
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ISSN:1360-9947
1460-2407
DOI:10.1093/molehr/gas019