ArticleReproductive sciences (Thousand Oaks, Calif.)2022
AP-1 Subunit JUNB Promotes Invasive Phenotypes in Endometriosis.
Article in Reproductive sciences (Thousand Oaks, Calif.), 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 9 citations in OpenAlex.
- Review
- Profiling miRNA in salivary samples from subjects with endometriosis: a pilot study.Frontiers in molecular biosciences · 2026Article
- Transcriptome profiling reveals dysregulation of inflammatory and protein synthesis genes in PCOS.Scientific reports · 2024Article
- Identification of New Markers of Angiogenic Sprouting Using Transcriptomics: New Role for RND3.Arteriosclerosis, thrombosis, and vascular biology · 2024Article
- The roles of chromatin regulatory factors in endometriosis.Journal of assisted reproduction and genetics · 2024Review
- Uterine Collagen Cross-Linking: Biology, Role in Disorders, and Therapeutic Implications.Reproductive sciences (Thousand Oaks, Calif.) · 2024Review
- PIK3CA mutation in endometriotic epithelial cells promotes viperin-dependent inflammatory response to insulin.Reproductive biology and endocrinology : RB&E · 2023Article
- Role of GLI1 in Hypoxia-Driven Endometrial Stromal Cell Migration and Invasion in Endometriosis.Computational and mathematical methods in medicine · 2022Article
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
Abstract
Endometriosis is a disease defined by the presence of abnormal endometrium at ectopic sites, causing pain and infertility in 10% of women. Mutations in the chromatin remodeling protein ARID1A (AT-rich interactive domain-containing protein 1A) have been identified in endometriosis, particularly in the more severe deep infiltrating endometriosis and ovarian endometrioma subtypes. ARID1A has been shown to regulate chromatin at binding sites of the Activator Protein 1 (AP-1) transcription factor, and AP-1 expression has been shown in multiple endometriosis models. Here, we describe a role for AP-1 subunit JUNB in promoting invasive phenotypes in endometriosis. Through a series of knockdown experiments in the 12Z endometriosis cell line, we show that JUNB expression in endometriosis promotes the expression of epithelial-to-mesenchymal transition genes co-regulated by ARID1A including transcription factors SNAI1 and SNAI2, cell adhesion molecules ICAM1 and VCAM1, and extracellular matrix remodelers LOX and LOXL2. In highly invasive ARID1A-deficient endometriotic cells, co-knockdown of JUNB is sufficient to suppress invasion. These results suggest that AP-1 plays an important role in the progression of invasive endometriosis, and that therapeutic inhibition of AP-1 could prevent the occurrence of deep infiltrating endometriosis.
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Registered trials
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