Lowered expression of CCN5 in endometriotic tissues promotes proliferation, migration and invasion of endometrial stromal cells.
10.12122/j.issn.1673-4254.2022.01.10
- Author:
Hong CAI
1
;
Mian LIU
1
;
Miao Ling LIN
1
;
Hong LI
1
;
Lang SHEN
1
;
Song QUAN
1
Author Information
1. Department of Obstetrics and Gynecology, Nanfang Hospital, Southern Medical University, Guangzhou 510515, China.
- Publication Type:Journal Article
- Keywords:
CCN5;
endometriosis;
epithelial-mesenchymal transition;
human endometrial stromal cell;
invasion;
migration;
proliferation
- MeSH:
Cell Movement;
Cell Proliferation;
Endometriosis/metabolism*;
Endometrium/metabolism*;
Epithelial Cells;
Epithelial-Mesenchymal Transition;
Female;
Humans;
Stromal Cells
- From:
Journal of Southern Medical University
2022;42(1):86-92
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVE:To explore the expression of CCN5 in endometriotic tissues and its impact on proliferation, migration and invasion of human endometrial stromal cells (HESCs).
METHODS:We collected ovarian endometriosis samples from 20 women receiving laparoscopic surgery and eutopic endometrium samples from 15 women undergoing IVF-ET for comparison of CCN5 expression. Cultured HESCs were transfected with a recombinant adenovirus Ad-CCN5 for CCN5 overexpression or with a CCN5-specific siRNA for knocking down CCN5 expression, and the changes of cell proliferation, migration and invasion were evaluated using CCK-8 assay, wound healing assay and Transwell chamber assay. RT-qPCR and Western blotting were used to examine the expression levels of epithelial-mesenchymal transition (EMT) markers including E-cadherin, N-cadherin, Snail-1 and vimentin in HESCs with CCN5 overexpression or knockdown.
RESULTS:CCN5 expression was significantly decreased in ovarian endometriosis tissues as compared with eutopic endometrium samples (P < 0.01). CCN5 overexpression obviously inhibited the proliferation, migration and invasion of HESCs, significantly increased the expression of E-cadherin and decreased the expressions of N-cadherin, Snail-1 and vimentin (P < 0.01). CCN5 knockdown significantly enhanced the proliferation, migration and invasion of HESCs and produced opposite effects on the expressions of E-cadherin, N-cadherin, Snail-1 and vimentin (P < 0.01).
CONCLUSION:CCN5 can regulate the proliferation, migration and invasion of HESCs and thus plays an important role in EMT of HESCs, suggesting the potential of CCN5 as a therapeutic target for endometriosis.
