FOXQ1 promotes endometriosis development by enhancing mitochondrial function

article OA: gold CC0
AI-generated summary by gemini-2.5-flash-lite, 2026-07-17

FOXQ1 expression is elevated in endometriosis lesions and enhances mitochondrial function to promote inflammation, proliferation, invasion, and migration of endometrial cells.

One-sentence paraphrase of the abstract; not a substitute for reading it. No clinical advice. How this works

AI-generated deep summary by qwen3.7-flash, 2026-08-13 · read from full text

This study investigated the role of FOXQ1 in endometriosis pathogenesis by analyzing tissue samples from 76 patients and conducting functional assays on human endometrial epithelial cells. The researchers found that FOXQ1 expression was significantly elevated in endometriotic lesions compared to controls, where it enhanced mitochondrial function through increased ATP production and reactive oxygen species levels. This upregulation of mitochondrial activity subsequently promoted cellular proliferation, invasion, and migration while inhibiting apoptosis and stimulating pro-inflammatory cytokine release. This paper is centrally about endometriosis — specifically exploring how FOXQ1-driven mitochondrial enhancement contributes to lesion progression and inflammatory responses.

Read from the paper's body, not the abstract. Not a substitute for reading the paper. No clinical advice. How this works

Abstract

BACKGROUND: Endometriosis (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. METHODS: Eutopic 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. RESULTS: The 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. CONCLUSIONS: FOXQ1 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.
Full text 5,232 characters · extracted from oa-html · 5 sections · click to expand

Abstract

Background Endometriosis (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.

Methods

Eutopic 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.

Results

The 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.

Conclusions

FOXQ1 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. Similar content being viewed by others Abbreviations - EMs: - Endometriosis - RT-qPCR: - Reverse transcription-quantitative PCR - mtDNA: - Mitochondrial DNA - ROS: - Reactive oxygen species - OCR: - Oxygen consumption rate - hEECs: - Human endometrial epithelial cells - MMP: - Matrix metalloproteinase - FACS: - Fluorescence-activated cell sorting - ROC: - Receiver operating characteristic - ESCs: - Ectopic endometrial stromal cells

Acknowledgements

We would like to thank Editage (www.editage.com) for English language editing. Funding This 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). Author information Authors and Affiliations Corresponding author Ethics declarations Conflict of interests The authors report no conflict of interest. Ethics approval and consent to participate This 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. Consent for publication Not applicable. 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 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 Liu, 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 Received: Accepted: Published: DOI: https://doi.org/10.1186/s40659-026-00698-7

Text is read by the "Ask this paper" AI Q&A widget below. Extraction quality varies by source — PMC NXML preserves structure cleanly, OA-HTML may include some navigation residue, and OA-PDF can have broken hyphenation. The publisher copy (via DOI) is the canonical version.

My notes (saved in your browser only)

Ask this paper AI returns verbatim quotes from the full text · source: oa-html

Answers must be backed by verbatim quotes from this paper's full text. Hallucinated quotes are dropped automatically; if no verbatim passage answers the question, we say so. How this works

Citation neighborhood (no data yet)

We don't have any in-corpus citations linked to this paper yet. This is a recent paper (2026) — citers typically take a year or two to land, and the OpenAlex reference graph may still be filling in.

SciLite annotations

organisms 1
human
chemicals 2
oxygen oxygen

Source provenance

europepmc
last seen: 2026-08-29T06:12:09.280863+00:00
openalex
last seen: 2026-08-29T06:04:16.107210+00:00
pubmed
last seen: 2026-08-29T06:06:05.423075+00:00
scilite
last seen: 2026-07-19T09:54:07.271699+00:00
License: CC0 · commercial use OK