LINC00702 promotes the proliferative, migratory and invasive phenotypes of endometrial stromal cells in endometriosis via the miR-103a-3p/FGF2 ceRNA axis

Background To investigate the expression pattern of LINC00702 in endometriosis and explore its regulatory role and molecular mechanism in endometrial stromal cells (ESCs).

Eutopic 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.

LINC00702 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.

LINC00702 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. Similar content being viewed by others

Not applicable. Funding The authors declare that no funds, grants, or other support was received during the preparation of this manuscript. Author information Authors and Affiliations Corresponding author Ethics declarations Ethics approval and consent to participate Written 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. Consent for publication Not applicable. Competing interests The authors declare no competing interests. Additional information Publisher’s note Springer Nature remains neutral with regard to jurisdictional claims in published maps and institutional affiliations. Rights and permissions Open 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. About this article Cite this article Luo, 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 Received: Accepted: Published: DOI: https://doi.org/10.1186/s41065-026-00759-7