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

Qiao-Mei Zheng, Qiaomei Zheng, Jingjing Lu, Jing-Jing Lu, Jing Zhao, Xuan Wei, Lu Wang, Peishu Liu
BioMed research international · 2016 · vol. 2016 , pp. 1–8 · doi:10.1155/2016/9842619 · PMID:27034956 · PMC4808541 · W2296595142
article OA: gold CC0 ⤵ 14 in-corpus citations
📄 Open PDF View on OpenAlex View on PubMed View at publisher
⚙ AI-generated summary by claude@2026-06, 2026-06-07 ⓘ

Periostin treatment enhanced endometrial epithelial cell migration, invasion, and epithelial-mesenchymal transition by upregulating the ILK-Akt signaling pathway.

One-sentence paraphrase of the abstract; not a substitute for reading it. No clinical advice. How this works

Abstract

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.

My notes (saved in your browser only)

Condition tags

endometriosis

MeSH descriptors

Cell Adhesion Molecules Endometriosis Epithelial-Mesenchymal Transition Oncogene Protein v-akt Protein Serine-Threonine Kinases Cell Adhesion Molecules Cell Adhesion Molecules Cell Adhesion Molecules Cell Line, Tumor Cell Movement Cell Movement Cell Proliferation Cell Proliferation Endometrial Stromal Tumors Endometrial Stromal Tumors Endometrial Stromal Tumors Endometriosis Endometriosis Endometriosis Endometrium

Citation neighborhood

Papers in the corpus that this work cites (lower rings, blue) and that cite this one (upper rings, green). Dot size scales with the paper's in-corpus citation count — bigger dot = more influential within the endo/adeno field. Click a dot to open that paper. [ expand to 2 hops ] — adds papers reached through this work's immediate citers/citees. Heavier; up to 60 extra dots.

References (41)

Cited by (14)

Source provenance

europepmc
last seen: 2026-06-11T06:19:48.454388+00:00
openalex
last seen: 2026-06-10T17:14:06.276822+00:00
pubmed
last seen: 2026-05-13T22:21:07.355239+00:00
License: CC0 · commercial use OK