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Background <p>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.</p> Methods <p>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.</p> Results <p>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.</p> Conclusions <p>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.</p>

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FOXQ1 promotes endometriosis development by enhancing mitochondrial function

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年7月7日

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  • Yu Liu,
  • Mei Chi,
  • Yan Lei,
  • Jing Jin,
  • Xiaojing Lei,
  • Shu Zhang,
  • Qingmei Guan,
  • Ling Zhang,
  • Xin Du

摘要

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.