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

• Published in: BioMed research international Vol. 2016; no. 2016; pp. 1 - 8
• Main Authors: Wang, Lu, Wei, Xuan, Zhao, Jing, Lu, Jingjing, Zheng, Qiao-mei, Liu, Pei-shu
• Format: Journal Article
• Language: English
• Published: Cairo, Egypt Hindawi Publishing Corporation 01.01.2016; Hindawi Limited
• Subjects: Cell adhesion & migration; Cell Adhesion Molecules - antagonists & inhibitors; Cell Adhesion Molecules - genetics; Cell Adhesion Molecules - metabolism; Cell Line, Tumor; Cell Movement - genetics; Cell Proliferation - genetics; Endometrial Stromal Tumors - genetics; Endometrial Stromal Tumors - pathology; Endometriosis; Endometriosis - genetics; Endometriosis - metabolism; Endometriosis - pathology; Endometrium - metabolism; Endometrium - pathology; Epithelial Cells - metabolism; Epithelial Cells - pathology; Epithelial-Mesenchymal Transition - genetics; Extracellular matrix; Female; Gene Expression Regulation, Neoplastic; Gynecology; Humans; Kinases; Ligands; Liver cancer; Metastasis; Neoplasm Invasiveness - genetics; Neoplasm Invasiveness - pathology; Obstetrics; Oncogene Protein v-akt - biosynthesis; Oncogene Protein v-akt - genetics; Pathogenesis; Phosphorylation; Protein-Serine-Threonine Kinases - biosynthesis; Protein-Serine-Threonine Kinases - genetics; Roles; Signal Transduction - genetics
• ISSN: 2314-6133; 2314-6141
• DOI: 10.1155/2016/9842619

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.