摘要
Osteopontin (OPN) isoforms, including OPNb and OPNc, promote malignancy and may contribute to the pathogenesis of endometriosis, a benign disorder with multiple characteristics resembling malignant tumors. In our experiments, OPNb and OPNc were significantly overexpressed in both endometriosis and adenomyosis compared to the normal endometrium. Upregulation of CD44v and the epithelial–mesenchymal transition (EMT) process was also present in endometriotic lesions. Overexpression of OPNb and OPNc splicing variants in endometriotic cells evoked morphological changes, actin remodeling, cell proliferation, cell migration, and EMT through binding OPN ligand receptors CD44 and αvβ3, subsequently activating the PI3K and NF-ĸB pathways. We elucidated the causal role of OPN splice variants in regulating endometriotic cell growth, which may promote the development of OPN-targeted therapies for patients suffering from endometriotic disorders.
原文 | 英語 |
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文章編號 | 15328 |
期刊 | International journal of molecular sciences |
卷 | 23 |
發行號 | 23 |
DOIs | |
出版狀態 | 已發佈 - 12月 2022 |
ASJC Scopus subject areas
- 催化
- 分子生物學
- 光譜
- 電腦科學應用
- 物理與理論化學
- 有機化學
- 無機化學