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Endometrial stromal cell proteomic analysis reveals LIM and SH3 protein 1 (LASP1) plays important roles in the progression of adenomyosis

Authors :
Yang Zou
Ouping Huang
Jun Liu
Jiang-Yan Zhou
Xiao-Qun Yuan
Xiao-Yun Xu
Liqun Wang
Yulan Yi
Shu-Fen Fang
Jiu-Bai Guo
Zeng-Ming Li
Fa-Ying Liu
Bianna Cao
Source :
Molecular Human Reproduction. 27
Publication Year :
2021
Publisher :
Oxford University Press (OUP), 2021.

Abstract

Adenomyosis is one of the most common gynecological disorders that the molecular events underlying its pathogenesis remain not fully understood. Prior studies have shown that endometrial stromal cells (ESCs) played crucial roles in the pathogenesis of adenomyosis. In this study, we utilized two-dimensional gel electrophoresis combined with protein identification by mass spectrometry (2D/MS) proteomics analysis to compare the differential protein expression profile between the paired eutopic and ectopic ESCs (EuESCs and EcESCs) in adenomyosis, and a total of 32 significantly altered protein spots were identified. Among which, the expression of LIM and SH3 protein 1 (LASP1) was increased significantly in EcESCs compared to EuESCs. Immunohistochemical assay showed that LASP1 was overexpressed in the stromal cells of ectopic endometriums compared to eutopic endometriums; further functional analyses revealed that LASP1 overexpression could enhance cell proliferation, migration and invasion of EcESCs. Furthermore, we also showed that the dysregulated expression of LASP1 in EcESCs was associated with DNA hypermethylation in the promoter region of the LASP1 gene. However, the detailed molecular mechanisms of enhancing cell proliferation, invasion and migration caused by upregulated LASP1 in adenomyosis needs further study. For the first time, our data suggested that LASP1 plays important roles in the pathogenesis of adenomyosis, and could serve as a prognostic biomarker of adenomyosis.

Details

ISSN :
14602407 and 13609947
Volume :
27
Database :
OpenAIRE
Journal :
Molecular Human Reproduction
Accession number :
edsair.doi.dedup.....b50a48e07bb3b974abd58ce1d15278f4