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Periostin Facilitates the Epithelial-Mesenchymal Transition of Endometrial
Epithelial Cells through ILK-Akt Signaling Pathway
#MMPMID27034956
Zheng QM
; Lu JJ
; Zhao J
; Wei X
; Wang L
; Liu PS
Biomed Res Int
2016[]; 2016
(?): 9842619
PMID27034956
show ga
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.
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