{"paper_id":"985dc656-b1cf-4891-8cf8-63fafafa170b","body_text":"Abstract\nBackground\nEndometriosis (EMs) is a pathological condition characterized by the ectopic growth of endometrial tissue outside the uterine cavity. This study aimed to investigate the role of FOXQ1 in the pathogenesis of EMs, particularly through its regulation of mitochondrial function.\nMethods\nEutopic endometrial, ovarian EMs, pelvic sidewall EMs, and bowel EMs samples were obtained from 76 patients undergoing laparoscopic or hysteroscopic surgery. The expression levels of FOXQ1 in EMs tissues were determined using reverse transcription-quantitative PCR (RT-qPCR) and western blot analysis. Furthermore, the mRNA expression levels of pro-inflammatory cytokines, including interleukin (IL)-6, interleukin (IL)-1β, tumor necrosis factor (TNF)-α, and interleukin (IL)-8, were quantified in FOXQ1 overexpression (OE) and FOXQ1 knockdown (siFOXQ1) groups using RT-qPCR. Mitochondrial function in these groups, using primary human endometrial epithelial cells (hEECs), was evaluated by assessing mitochondrial DNA (mtDNA) content, ATP production, reactive oxygen species (ROS) levels, oxygen consumption rate (OCR), and MitoTracker staining. The in vitro effects of FOXQ1 on EMs were further examined in hEECs by analyzing cellular apoptosis, proliferation, invasion, and migration.\nResults\nThe expression of FOXQ1 was markedly elevated in endometriotic lesions, such as those on the pelvic sidewall and bowel, compared to control samples, with localization specifically observed in endometrial epithelial cells. Functional assays conducted on hEECs demonstrated that overexpression of FOXQ1 inhibited apoptosis, upregulated critical inflammatory cytokines (IL-6, IL-1β, TNF-α, IL-8), and promoted cellular proliferation, invasion, and migration. These effects appear to be mediated by enhanced mitochondrial function, as indicated by increased mtDNA content, ATP production, ROS levels, OCR, and MitoTracker signal. Conversely, the group treated with siFOXQ1 exhibited the opposite effects. The receiver operating characteristic curve analysis revealed that the area under the curve for FOXQ1 was 0.8784.\nConclusions\nFOXQ1 facilitates the progression of endometriosis by enhancing mitochondrial function, which subsequently stimulates inflammatory responses and promotes critical cellular processes such as proliferation, invasion, and migration.\nSimilar content being viewed by others\nAbbreviations\n- EMs:\n-\nEndometriosis\n- RT-qPCR:\n-\nReverse transcription-quantitative PCR\n- mtDNA:\n-\nMitochondrial DNA\n- ROS:\n-\nReactive oxygen species\n- OCR:\n-\nOxygen consumption rate\n- hEECs:\n-\nHuman endometrial epithelial cells\n- MMP:\n-\nMatrix metalloproteinase\n- FACS:\n-\nFluorescence-activated cell sorting\n- ROC:\n-\nReceiver operating characteristic\n- ESCs:\n-\nEctopic endometrial stromal cells\nAcknowledgements\nWe would like to thank Editage (www.editage.com) for English language editing.\nFunding\nThis work was supported by the Maternal and Child Health Hospital of Hubei Province Research Project (grant number: 2023SFYM002). Natural Science Foundation of Hubei Province of China (2024AFB1062).\nAuthor information\nAuthors and Affiliations\nCorresponding author\nEthics declarations\nConflict of interests\nThe authors report no conflict of interest.\nEthics approval and consent to participate\nThis study was approved by the Ethics Committee of the Medical College of the Provincial Maternal and Child Health Hospital (IORGNo:2022IEC061). This study adhered to the principles of the Declaration of Helsinki. All participants agreed to this study and signed informed consent forms.\nConsent for publication\nNot applicable.\nAdditional information\nPublisher’s note\nSpringer Nature remains neutral with regard to jurisdictional claims in published maps and institutional affiliations.\nSupplementary Information\nBelow is the link to the electronic supplementary material.\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\nLiu, Y., Chi, M., Lei, Y. et al. FOXQ1 promotes endometriosis development by enhancing mitochondrial function. Biol Res (2026). https://doi.org/10.1186/s40659-026-00698-7\nReceived:\nAccepted:\nPublished:\nDOI: https://doi.org/10.1186/s40659-026-00698-7","source_license":"CC0","license_restricted":false}