[Lowered expression of CCN5 in endometriotic tissues promotes proliferation, migration and invasion of endometrial stromal cells].

H Cai, Haibo Cai, Cai H, M Liu, Liu M, Minghui Liu, M Lin, Lin M, Min‐Hsuan Lin, H Li, Li H, L Shen, Lei Shen, Shen L, S Quan, Song Quan, Quan S
Nan fang yi ke da xue xue bao = Journal of Southern Medical University · 2022 · vol. 42(1) , pp. 86–92 · doi:10.12122/j.issn.1673-4254.2022.01.10 · PMID:35249874 · PMC8901405 · W4220853381
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⚙ AI-generated summary by gemini-2.5-flash-lite, 2026-06-07 ⓘ

Lowered expression of CCN5 in endometriotic tissues promotes proliferation, migration, and invasion of endometrial stromal cells by regulating epithelial-mesenchymal transition.

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⚙ AI-generated deep summary by claude@2026-06, 2026-06-07 · read from full text ⓘ

The study examined CCN5 expression in ovarian endometriosis tissue and compared it with CCN5 levels in normally located endometrial tissues, then tested how altered CCN5 affected human endometrial stromal cells (HESCs). Using recombinant adenovirus to overexpress CCN5 and si-RNA to knock it down, the authors measured HESC proliferation (CCK-8), migration and invasion (wound-healing and Transwell assays), and EMT marker changes (Western blot for E-cadherin, N-cadherin, Snail-1, and vimentin). CCN5 was significantly lower in endometriotic tissues than in controls, and overexpression inhibited HESC proliferation, migration, invasion, and EMT, whereas CCN5 knockdown enhanced these malignant behaviors and promoted EMT. The paper does not state specific limitations such as sample size or whether findings were validated in vivo. This paper is centrally about endometriosis — it directly links lowered CCN5 expression in endometriotic tissues to altered proliferation, migration, invasion, and EMT in HESCs, implicating CCN5 in endometriosis progression.

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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: < 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.
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南方医科大学学报 ›› 2022, Vol. 42 ›› Issue (1): 86-92.doi: 10.12122/j.issn.1673-4254.2022.01.10 蔡 虹，刘 勉，林妙玲，李 红，沈 朗，全 松 - 南方医科大学南方医院妇产科，广东 广州 510515 CAI Hong, LIU Mian, LIN Miaoling, LI Hong, SHEN Lang, QUAN Song - Department of Obstetrics and Gynecology, Nanfang Hospital, Southern Medical University, Guangzhou 510515, China 摘要： 目的 分析CCN5在卵巢子宫内膜异位囊肿组织中的表达情况，探究其对子宫内膜基质细胞（HESCs）增殖、迁移和侵袭能力的影响。方法 收集并比较卵巢子宫内膜异位症患者组织与正常对照组在位子宫内膜组织中CCN5的表达水平；利用重组腺病毒Ad-CCN5构建过表达CCN5的人子宫内膜基质细胞；采用si-RNA构建敲低CCN5的人子宫内膜基质细胞。利用CCK-8实验检测不同表达水平CCN5对HESCs细胞增殖能力的影响；划痕实验、Transwell小室侵袭实验检测不同表达水平CCN5对HESCs细胞迁移与侵袭能力的影响；Western blot检测不同处理组 HESCs中上皮-间充质转化（EMT）标记物 E-cadherin、N-cadherin，snail-1和vimentin的表达水平。结果 卵巢子宫内膜异位组织中CCN5的表达水平较正常对照组在位子宫内膜显著降低（P<0.01）；过表达CCN5可以抑制HESCs的增殖、迁徙及侵袭能力；EMT标记物E-cadherin表达升高，N-cadherin、Snail-1 和Vimentin表达降低，EMT受到显著抑制（P<0.01）。而敲低CCN5的表达可以显著增强HESCs的增殖、迁移及侵袭（P<0.01），降低E-cadherin表达，升高N-cadherin、Snail-1和Vimentin表达，促进HESCs发生EMT转化。结论 CCN5在卵巢子宫内膜异位组织中的表达水平显著降低，可能通过调控HESCs的增殖、迁移与侵袭能力及影响EMT，在卵巢子宫内膜异位症的发生发展中发挥重要作用。

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Condition tags

endometriosis

MeSH descriptors

Endometriosis Endometriosis Cell Movement Cell Proliferation Endometrium Endometrium Epithelial Cells Epithelial-Mesenchymal Transition Female Humans Stromal Cells

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