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CD147 Induces Epithelial-to-Mesenchymal Transition by Disassembling Cellular Apoptosis Susceptibility Protein/E-Cadherin/β-Catenin Complex in Human Endometriosis.

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机构： [1]Epithelial Cell Biology Research Center,School of Biomedical Sciences, Faculty of Medicine, The Chinese University of Hong Kong, Shatin, Hong Kong [2]the Institute of Biomedical and Pharmaceutical Sciences,Guangdong University of Technology, People’s Republic of China [3]the Sichuan UniversityeThe Chinese University of Hong Kong Joint Laboratory for Reproductive Medicine,West China Second University Hospital, Sichuan University, Sichuan, People’s Republic of China [4]University of California, San Francisco, San Francisco, CA.

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Epithelial-to-mesenchymal transition (EMT) is postulated to be a prerequisite for the establishment of endometriosis (EMS), a common reproductive disorder in women. Our previous studies have demonstrated the elevated expression of transmembrane glycoprotein CD147 and its prosurvival effect on abnormal cells in endometriosis. Intriguingly, CD147 is known to promote EMT in cancers. However, the involvement of CD147 in EMT during the establishment of endometriosis remains incompletely understood. We found that CD147 promotes EMT in human endometrial adenocarcinoma cell line Ishikawa. We identified a novel CD147-interacting partner, cellular apoptosis susceptibility protein (CAS), which stabilized the interaction between E-cadherin (E-cad) and β-catenin (β-cat) by forming the CAS/E-cad/β-cat complex. Down-regulation of CAS led to the release and nuclear translocation of β-cat from E-cad, resulting in the overexpression of the EMT-promoting gene SNAIL. Interestingly, overexpression of CD147 impaired the interaction between CAS and E-cad and triggered the release of β-cat from the CAS/E-cad/β-cat complex, which in turn led to EMT. Furthermore, CAS was down-regulated in EMS, with elevated levels of CD147 and nuclear β-cat. These findings suggest a previously undefined role of CAS in regulating EMT and reveal the involvement of a CD147-induced EMT signaling pathway in pathogenic progression of EMS. Copyright © 2018 American Society for Investigative Pathology. Published by Elsevier Inc. All rights reserved.

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出版当年[2018]版：

大类 | 2 区

医学

小类 | 2 区病理学

最新[2023]版：

大类 | 2 区医学

小类 | 2 区病理学

第一作者：

第一作者机构： [1]Epithelial Cell Biology Research Center,School of Biomedical Sciences, Faculty of Medicine, The Chinese University of Hong Kong, Shatin, Hong Kong [4]University of California, San Francisco, San Francisco, CA.

通讯作者：

通讯机构： [1]Epithelial Cell Biology Research Center,School of Biomedical Sciences, Faculty of Medicine, The Chinese University of Hong Kong, Shatin, Hong Kong [2]the Institute of Biomedical and Pharmaceutical Sciences,Guangdong University of Technology, People’s Republic of China [3]the Sichuan UniversityeThe Chinese University of Hong Kong Joint Laboratory for Reproductive Medicine,West China Second University Hospital, Sichuan University, Sichuan, People’s Republic of China [*1]Institute of Biomedical and Pharmaceutical Sciences, Guangdong University of Technology, No. 100, Waihuan Xi Road, Guangzhou Higher Education Mega Center, People’s Republic of China, 510006 [*2]Epithelial Cell Biology Research Center, School of Biomedical Sciences, Faculty of Medicine, The Chinese University of Hong Kong, Shatin, Hong Kong.

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