ArticleReproductive sciences (Thousand Oaks, Calif.)2019
The Essential Role of GATA6 in the Activation of Estrogen Synthesis in Endometriosis.
Article in Reproductive sciences (Thousand Oaks, Calif.), 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
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Who cites it
26 citing papers in PubMed, 36 citations in OpenAlex.
- Cancer-like Hallmarks of Endometriosis: The Role of Estrogen Signaling and Stem Cell Plasticity.International journal of molecular sciences · 2026Review
- miR-196b inhibits tumor proliferation and metastasis by targeting GATA6 in endometrial cancer.Biology direct · 2026Article
- The hypoxia-epigenetics-ncRNA axis in endometriosis: from molecular cascades to self-sustaining pathogenic circuits.Frontiers in endocrinology · 2026Review
- Harnessing diet to modulate inflammation and symptom progression in endometriosis.Frontiers in nutrition · 2026Review
- Endometriosis and ovulatory menstruation: beyond the Sampson principle.The Journal of clinical investigation · 2025Review
- Macrophage Plasticity and Extracellular Vesicles in Endometriosis: Immunopathology and Therapeutic Perspectives.Reproductive sciences (Thousand Oaks, Calif.) · 2025Review
- Epigenetic regulation of nuclear receptors: Implications for endocrine-related diseases and therapeutic strategies.Genes & diseases · 2025Review
- Blocking GATA6 Alleviates Pyroptosis and Inhibits Abdominal Wall Endometriosis Lesion Growth Through Inactivating the PI3K/AKT Pathway.Cell biochemistry and biophysics · 2025Article
- Identification of distinct stool metabolites in women with endometriosis for non-invasive diagnosis and potential for microbiota-based therapies.Med (New York, N.Y.) · 2025Article
- Leveraging epigenetic aberrations in the pathogenesis of endometriosis: from DNA methylation to non-coding RNAs.Frontiers in genetics · 2025Review
- Immunohistochemical Analysis of GATA2 Expression in Endometrium and its Relationship with Hormone Receptor Expression in Benign and Premalignant Endometrial Disorders.Reproductive sciences (Thousand Oaks, Calif.) · 2024Article
- Impaired bone morphogenetic protein (BMP) signaling pathways disrupt decidualization in endometriosis.Communications biology · 2024Article
- Therapeutic effects of Huayu Jiedu formula on endometriosis via downregulating GATA 6 expression.Heliyon · 2024Article
- Impaired bone morphogenetic protein (BMP) signaling pathways disrupt decidualization in endometriosis.Research square · 2023Article
- Identification of potential diagnostic biomarkers and therapeutic targets for endometriosis based on bioinformatics and machine learning analysis.Journal of assisted reproduction and genetics · 2023Article
- Deciphering a shared transcriptomic regulation and the relative contribution of each regulator type through endometrial gene expression signatures.Reproductive biology and endocrinology : RB&E · 2023Article
- New concepts on the etiology of endometriosis.The journal of obstetrics and gynaecology research · 2023Article
- Endometriosis Stem Cells as a Possible Main Target for Carcinogenesis of Endometriosis-Associated Ovarian Cancer (EAOC).Cancers · 2022Review
- Current Knowledge on Endometriosis Etiology: A Systematic Review of Literature.International journal of women's health · 2021Review
- Identification of Key Genes and Pathways associated with Endometriosis by Weighted Gene Co-expression Network Analysis.International journal of medical sciences · 2021Article
Corrections and comments
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
Endometriotic stromal cells synthesize estradiol via the steroidogenic pathway. Nuclear receptor subfamily 5, group A, member 1 (NR5A1) is critical, but alone not sufficient, in activating this cascade that involves at least 5 genes. To evaluate whether another transcription factor is required for the activation of this pathway, we examined whether GATA Binding Protein 6 (GATA6) can transform a normal endometrial stromal cell (NoEM) into an endometriotic-like cell by conferring an estrogen-producing phenotype. We ectopically expressed GATA6 alone or with NR5A1 in NoEM or silenced these transcription factors in endometriotic stromal cells (OSIS) and assessed the messenger RNAs or proteins encoded by the genes in the steroidogenic cascade. Functionally, we assessed the effects of GATA6 expression or silencing on estradiol formation. In OSIS, GATA6 was necessary for catalyzing the conversion of progesterone to androstenedione (CYP17A1; P < .05). In NoEM, ectopic expression of GATA6 was essential for converting pregnenolone to estrogen (HSD3B2, CYP17A1, and CYP19A1; P < .05). However, simultaneous ectopic expression of both GATA6 and NR5A1 was required and sufficient to confer induction of all 5 genes and their encoded proteins that convert cholesterol to estrogen. Functionally, only simultaneous knockdown of GATA6 and NR5A1 blocked estradiol formation in OSIS ( P < .05). The presence of both transcription factors was required and sufficient to transform endometrial stromal cells into endometriotic-like cells that produced estradiol in large quantities ( P < .05). In summary, GATA6 alone is essential but not sufficient for estrogen formation in endometriosis. However, simultaneous addition of GATA6 and NR5A1 to an endometrial stromal cell is sufficient to transform it into an endometriotic-like cell, manifested by the activation of the estradiol biosynthetic cascade.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.