Periostin Facilitates the Epithelial-Mesenchymal Transition of Endometrial Epithelial Cells through ILK-Akt Signaling Pathway.

Although periostin was confirmed to facilitate the pathogenesis of endometriosis by enhancing the migration, invasion, and adhesion of human endometrial stromal cells (ESCs), its effect on the endometrial epithelial cells (EECs) is still unknown. The current study aimed to determine whether periosti...

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Publicado en:BioMed Research International Vol. 2016; pp. 1 - 9
Autores principales: Zheng, Qiao-mei, Lu, Jing-jing, Zhao, Jing, Wei, Xuan, Wang, Lu, Liu, Pei-shu
Formato: pictorial research tables/charts Journal Article
Publicado: Wiley-Blackwell 3/13/2016
Acceso en línea:Ver este registro en EBSCOhost
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      dt: 3/13/2016
      vid: 2016
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      pub: Wiley-Blackwell
      place: Malden, Massachusetts
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        10.1155/2016/9842619
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        atl: Periostin Facilitates the Epithelial-Mesenchymal Transition of Endometrial Epithelial Cells through ILK-Akt Signaling Pathway.
      aug:
        au:
          Zheng, Qiao-mei
          Lu, Jing-jing
          Zhao, Jing
          Wei, Xuan
          Wang, Lu
          Liu, Pei-shu
        affil: Department of Obstetrics and Gynecology, Qilu Hospital of Shandong University, 107 Wenhua Xi Road, Jinan, Shandong 250012, China
      sug:
        subj:
          Signal Transduction
          Endometrium
          Epithelial Cells
          Cell Physiology
          Proteins Administration and Dosage
          Extracellular Space
          Endometriosis Pathology
          Human
          Cell Culture Techniques
          Female
          Cell Adhesion Molecules Drug Effects
          Cytoskeletal Proteins
          Phosphotransferases
          Adult
          China
          Biological Assay
          Blotting, Western
          Data Analysis Software
          Descriptive Statistics
          T-Tests
          One-Way Analysis of Variance
          P-Value
          Cell Movement
          Funding Source
          Adult: 19-44 years
          Female
      ab: Although periostin was confirmed to facilitate the pathogenesis of endometriosis by enhancing the migration, invasion, and adhesion of human endometrial stromal cells (ESCs), its effect on the endometrial epithelial cells (EECs) is still unknown. The current study aimed to determine whether periostin enhanced the epithelial-mesenchymal transition (EMT) of EECs. EECs were isolated from 12 women with endometriosis. The migration and invasion abilities of EECs were evaluated by transwell assays. Expressions of proteins were detected by western blot. After treatment with periostin, the migration and invasion abilities of EECs were enhanced. Additionally, E-cadherin and keratin were downregulated while N-cadherin and vimentin were upregulated in EECs. Simultaneously, levels of ILK, p-Akt, slug, and Zeb1 were all upregulated in EECs. After silencing the expression of ILK in EECs, levels of p-Akt, slug, Zeb1, N-cadherin, and vimentin were downregulated while E-cadherin and keratin were upregulated. Although periostin weakened the above effects in EECs after silencing the expression of ILK, it failed to induce the EMT of EECs. Thus, periostin enhanced invasion and migration abilities of EECs and facilitated the EMT of EECs through ILK-Akt signaling pathway. Playing a pivotal role in the pathogenesis of endometriosis, periostin may be a new clinical therapy target for endometriosis.
      pubtype: Academic Journal
      doctype:
        pictorial
        research
        tables/charts
        Journal Article
      ougenre: Article
    language: English
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