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

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. Similar content being viewed by others Data availability All data analyzed during this study will be made available on reasonable request. Code availability Not applicable. Change history 31 May 2024 A Correction to this paper has been published: https://doi.org/10.1007/s43032-024-01609-5

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We thank International Science Editing ( http://www.internationalscienceediting.com ) for editing this manuscript. Funding This work was supported by the Shandong Traditional Chinese Medicine Technology Project (Q-2022128) and the Weifang Health Commission Scientific Research Project (WFWSJK-2022–006). Author information Authors and Affiliations Contributions We express our gratitude to all authors for their valuable contributions. AJ, TY, ZW, QZ, and CZ were responsible for the design of the experiments. ZW, QZ, CZ, and JY were responsible for conducting the experiments. TY and AJ offered both experimental and analytical assistance. Reagents, materials, and analysis tools were contributed by TY. The responsibility of interpreting the data and writing the manuscript lies with ZW, QZ, and CZ. AJ conducted a thorough evaluation of the manuscript. Corresponding author Ethics declarations Ethics approval The ethics committee of the Affiliated Hospital of Shandong Second Medical University granted approval for all experiments involving human tissue samples (Approval number: Wyfy-2023-ky-280). Consent to participate Informed consent was obtained from each patient. Consent for publication All authors have agreed to publish the article. Conflict of interest There is no conflict of interest. Additional information Publisher's Note Springer Nature remains neutral with regard to jurisdictional claims in published maps and institutional affiliations. Supplementary Information Below is the link to the electronic supplementary material. Rights and permissions Springer Nature or its licensor (e.g. a society or other partner) holds exclusive rights to this article under a publishing agreement with the author(s) or other rightsholder(s); author self-archiving of the accepted manuscript version of this article is solely governed by the terms of such publishing agreement and applicable law. About this article Cite this article Wang, Z., Zhang, Q., Zhang, C. et al. CADM2 participates in endometriosis development by influencing the epithelial-mesenchymal transition. Reprod. Sci. 31, 3049–3057 (2024). https://doi.org/10.1007/s43032-024-01592-x Received: Accepted: Published: Version of record: Issue date: DOI: https://doi.org/10.1007/s43032-024-01592-x