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Background <p>Endometriosis is a hormonally responsive inflammatory disease with a recognized association with certain ovarian cancer subtypes. Gonadotropins are widely used in assisted reproductive technologies; however, their direct molecular effects on endometriotic tissue remain insufficiently characterized.</p> Objective <p>This study aimed to investigate the effects of gonadotropin treatment on molecular markers potentially associated with early carcinogenesis-related processes in endometriotic lesions, using a surgically induced rat model.</p> Methods <p>Twenty-two female Wistar Albino rats underwent surgical induction of endometriosis via autologous peritoneal implantation. The animals were randomly assigned to two groups: a control group receiving saline and a treatment group receiving gonadotropin (2&#xa0;IU/kg/day) for 14&#xa0;days. Following treatment, endometriotic lesions were excised and analyzed histologically and immunohistochemically for phosphatase and tensin homolog (PTEN), tumor protein 53 (TP53), and tumor necrosis factor-alpha (TNF-α) expression. Statistical analyses were performed using the Mann–Whitney U test based on non-parametric data distribution.</p> Results <p>Histopathological evaluation revealed no significant morphological differences between the groups. However, quantitative immunohistochemical analysis demonstrated that gonadotropin-treated rats exhibited markedly decreased PTEN (<i>p</i> &lt; 0.001) and TP53 (<i>p</i> = 0.001) expression, alongside a significant increase in TNF-α expression (<i>p</i> = 0.035) compared with controls (Table&#xa0;1<InternalRef RefID="Tab1">,</InternalRef> Figs. <InternalRef RefID="Fig5">5</InternalRef>, <InternalRef RefID="Fig6">6</InternalRef>). These alterations reflect early molecular changes involving tumor suppressor gene downregulation and pro-inflammatory cytokine upregulation.</p> Conclusion <p>These findings suggest that gonadotropin exposure may induce early molecular alterations in endometriotic tissue. Further translational and clinical studies are warranted to validate these findings in human populations.</p>

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Gonadotropin-Induced Molecular Alterations in Experimental Endometriosis: Downregulation of Tumor Suppressor Genes and Inflammatory Activation

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年2月2日

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  • Erol Karakaş,
  • Mehmet Dolanbay,
  • Mustafa Ermiş,
  • Hülya Akgün,
  • Arzu Hanım Yay,
  • Eda Köseoğlu,
  • Enes Karaman

摘要

Background

Endometriosis is a hormonally responsive inflammatory disease with a recognized association with certain ovarian cancer subtypes. Gonadotropins are widely used in assisted reproductive technologies; however, their direct molecular effects on endometriotic tissue remain insufficiently characterized.

Objective

This study aimed to investigate the effects of gonadotropin treatment on molecular markers potentially associated with early carcinogenesis-related processes in endometriotic lesions, using a surgically induced rat model.

Methods

Twenty-two female Wistar Albino rats underwent surgical induction of endometriosis via autologous peritoneal implantation. The animals were randomly assigned to two groups: a control group receiving saline and a treatment group receiving gonadotropin (2 IU/kg/day) for 14 days. Following treatment, endometriotic lesions were excised and analyzed histologically and immunohistochemically for phosphatase and tensin homolog (PTEN), tumor protein 53 (TP53), and tumor necrosis factor-alpha (TNF-α) expression. Statistical analyses were performed using the Mann–Whitney U test based on non-parametric data distribution.

Results

Histopathological evaluation revealed no significant morphological differences between the groups. However, quantitative immunohistochemical analysis demonstrated that gonadotropin-treated rats exhibited markedly decreased PTEN (p < 0.001) and TP53 (p = 0.001) expression, alongside a significant increase in TNF-α expression (p = 0.035) compared with controls (Table 1, Figs. 5, 6). These alterations reflect early molecular changes involving tumor suppressor gene downregulation and pro-inflammatory cytokine upregulation.

Conclusion

These findings suggest that gonadotropin exposure may induce early molecular alterations in endometriotic tissue. Further translational and clinical studies are warranted to validate these findings in human populations.