{"paper_id":"4ff68c1b-fc87-4ef6-96b6-305edb312e83","body_text":"Abstract\nBackground\nTo investigate the expression pattern of LINC00702 in endometriosis and explore its regulatory role and molecular mechanism in endometrial stromal cells (ESCs).\nMethods\nEutopic and ectopic tissues from 84 endometriosis patients and normal tissues from 72 controls were collected. Primary normal endometrial stromal cells (NESCs) and ectopic endometrial stromal cells (EcESCs) were isolated and cultured. LINC00702, miR-103a-3p, and FGF2 expression were detected by RT-qPCR. Cell proliferation, apoptosis, migration, and invasion were assessed by CCK-8, flow cytometry, and Transwell assays. Subcellular localization, dual-luciferase reporter assays, and rescue experiments were performed to validate the LINC00702/miR-103a-3p/FGF2 regulatory axis.\nResults\nLINC00702 was upregulated in ectopic endometrial tissues and EcESCs. Overexpression of LINC00702 enhanced the proliferative, anti‑apoptotic, migratory, and invasive phenotypes of NESCs, while silencing LINC00702 reversed these phenotypes in EcESCs. miR-103a-3p was downregulated in endometriosis and could reverse the regulatory effect of LINC00702 on ESCs. FGF2 was a direct target of miR-103a-3p, which was highly expressed in endometriosis and positively correlated with LINC00702. FGF2 knockdown reversed the effect of LINC00702 overexpression on NESCs, while FGF2 overexpression rescued the inhibitory effect of LINC00702 silencing on EcESCs.\nConclusion\nLINC00702 promotes proliferative, anti‑apoptotic, migratory, and invasive phenotypes of ESCs in endometriosis through the LINC00702/miR-103a-3p/FGF2 ceRNA regulatory axis, providing potential therapeutic targets for endometriosis treatment.\nSimilar content being viewed by others\nAcknowledgements\nNot applicable.\nFunding\nThe authors declare that no funds, grants, or other support was received during the preparation of this manuscript.\nAuthor information\nAuthors and Affiliations\nCorresponding author\nEthics declarations\nEthics approval and consent to participate\nWritten informed consent was obtained from all participants. The study protocol was approved by the Ethics Committee of Xinxiang Central Hospital (Ethics approval number: 2021-10-23) and the Research Institute and performed in line with the principles of the Declaration of Helsinki.\nConsent for publication\nNot applicable.\nCompeting interests\nThe authors declare no competing interests.\nAdditional information\nPublisher’s note\nSpringer Nature remains neutral with regard to jurisdictional claims in published maps and institutional affiliations.\nRights and permissions\nOpen Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated in a credit line to the data.\nAbout this article\nCite this article\nLuo, Y., Li, J., Yuan, M. et al. LINC00702 promotes the proliferative, migratory and invasive phenotypes of endometrial stromal cells in endometriosis via the miR-103a-3p/FGF2 ceRNA axis. Hereditas (2026). https://doi.org/10.1186/s41065-026-00759-7\nReceived:\nAccepted:\nPublished:\nDOI: https://doi.org/10.1186/s41065-026-00759-7","source_license":"CC0","license_restricted":false}