Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
. 2024 Oct;31(10):3049-3057.
doi: 10.1007/s43032-024-01592-x. Epub 2024 May 20.

CADM2 participates in endometriosis development by influencing the epithelial-mesenchymal transition

Zheng Wang #  1   2 , Qiqi Zhang #  1   2 , Chen Zhang #  2   3 , Jun Yan  1   2 , Tingting Yang  1 , Aifang Jiang  4
Affiliations

CADM2 participates in endometriosis development by influencing the epithelial-mesenchymal transition

Zheng Wang et al. Reprod Sci. 2024 Oct.

Erratum in

Abstract

Endometriosis (EM) is a common gynecologic condition that often leads to infertility in women of reproductive age. Cell adhesion molecule 2 (CADM2) is involved in maintaining cell adhesion and polarity, as well as suppressing tumors. However, the role and mechanism of CADM2 in endometriosis is unclear. Therefore, this study evaluated the expression levels of CADM2 and epithelial-mesenchymal transition (EMT)-related marker proteins (E-cadherin, α-SMA, and N-cadherin). Compared to normal endometrial tissue, CADM2 was expressed at low levels in ectopic endometrial tissue from patients with EM. We performed clone formation assays, wound healing assays, and Transwell cell invasion assays to investigate the effects of CADM2 on the biological behavior of endometriosis epithelial cells (11Z) and ectopic endometrial stromal cells (EESCs). The growth, migration, and invasion abilities of these cells were significantly inhibited by overexpression of CADM2. The results were reversed after the knockdown of CADM2. Finally, western blotting (WB) was utilized to detect the effect of CADM2 on EMT in endometriosis cells. CADM2 inhibited EMT in endometriosis cells. In conclusion, our study suggests that CADM2 is a negative regulator of endometriosis development and may inhibit endometriosis development by suppressing EMT.

Keywords: Cell adhesion molecule 2 (CADM2); Endometriosis; Epithelial-mesenchymal transition (EMT).

PubMed Disclaimer

Similar articles

See all similar articles

References

    1. Krina T, Zondervan DPCM, Stacey A, Missmer SD. Endometriosis. New Engl J Med. 2020;382(13):1244–56. - DOI
    1. Agostinis C, Balduit A, Mangogna A, et al. Immunological basis of the endometriosis: the complement system as a potential therapeutic target. Front Immunol. 2021;11:599117. - DOI - PubMed - PMC
    1. Bjedov S, Lvodylnxã LX, RãnrHãlq DD, et al. Endometriosis, pain and mental health. Psychiatria Danubina. 2021;33(Suppl 4):632–6. - PubMed
    1. Lagana AS, Garzon S, Gotte M, et al. The Pathogenesis of Endometriosis: Molecular and Cell Biology Insights. Int J Mol Sci. 2019;20(22):5615. - DOI - PubMed - PMC
    1. Sampson JA. Metastatic or embolic endometriosis, due to the menstrual dissemination of endometrial tissue into the venous circulation. Am J Pathol. 1927;3(2):93–110. - PubMed - PMC

LinkOut - more resources