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Related Experiment Video

Updated: Aug 14, 2025

Mouse Model of Surgically-induced Endometriosis by Auto-transplantation of Uterine Tissue
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Mouse Model of Surgically-induced Endometriosis by Auto-transplantation of Uterine Tissue

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Single-cell transcriptomic analysis of endometriosis.

Marcos A S Fonseca1,2, Marcela Haro1,2, Kelly N Wright3

  • 1Women's Cancer Research Program at the Samuel Oschin Comprehensive Cancer Center, Cedars-Sinai Medical Center, Los Angeles, CA, USA.

Nature Genetics
|January 9, 2023
PubMed

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Summary

This study created a cellular atlas of endometriosis, revealing distinct cellular and molecular signatures in diseased tissues. These findings highlight cellular reprogramming and inflammation in endometriosis and its link to ovarian cancer.

Area of Science:

  • Reproductive biology
  • Genomics
  • Oncology

Background:

  • Endometriosis is a prevalent gynecological condition causing chronic pain, infertility, and increased ovarian cancer risk.
  • Understanding the cellular and molecular basis of endometriosis is crucial for developing effective treatments.

Purpose of the Study:

  • To generate a comprehensive cellular atlas of endometriosis across various tissue types.
  • To identify cellular and molecular signatures associated with endometriosis and its progression.
  • To investigate the relationship between endometriosis and ovarian cancer at a cellular level.

Main Methods:

  • Single-cell RNA sequencing (scRNA-seq) of over 370,000 cells from endometriomas, endometriosis lesions, eutopic endometrium, ovaries, and peritoneum.
  • Comparative analysis of transcriptomes to identify distinct cellular and molecular profiles.

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  • Investigation of somatic mutations, such as ARID1A, and their impact on cellular behavior.

    • Main Results:

    • A detailed cellular atlas revealed differences in endometrial-type epithelial and stromal cells across tissue sites, indicating cellular restructuring and transcriptional reprogramming.
    • Endometrioma tissues exhibited dysregulated inflammatory pathways and complement protein upregulation in epithelial, stromal, and mesothelial cells.
    • Somatic ARID1A mutations were linked to increased pro-angiogenic and pro-lymphangiogenic factors and altered endothelial cell populations, including lymphatic endothelial cells.
    • Ciliated epithelial cell signatures were enriched in ovarian cancers, supporting the epidemiological link between endometriosis and ovarian cancer.

    Conclusions:

    • Endometriosis involves significant cellular and molecular alterations, including inflammation and transcriptional reprogramming.
    • Specific cellular signatures, like those in ciliated epithelial cells, may predispose individuals to ovarian cancer.
    • This cellular atlas provides a foundation for understanding endometriosis pathogenesis and identifying therapeutic targets.