ArticleeLife2022
Chromatin topology defines estradiol-primed progesterone receptor and PAX2 binding in endometrial cancer cells.
Article in eLife, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
12 citing papers in PubMed, 32 citations in OpenAlex.
- Endometrioid Intraepithelial Neoplasia in the Secretory Phase: Morphologic and Biomarker Diagnostic Features in a Common, Overlooked Setting.The American journal of surgical pathology · 2026Article
- Advances in the molecular mechanisms underlying progestin resistance in endometrial cancer.Fundamental research · 2025Review
- A distinct mechanism of epigenetic reprogramming silences PAX2 and initiates endometrial carcinogenesis.The Journal of clinical investigation · 2025Article
- Estrogen-induced chromatin looping changes identify a subset of functional regulatory elements.Genome research · 2025Article
- Unexpected nuclear hormone receptor and chromatin dynamics regulate estrous cycle dependent gene expression.Nucleic acids research · 2024Article
- Article
- Sex steroid hormones: an overlooked yet fundamental factor in oral homeostasis in humans.Frontiers in endocrinology · 2024Review
- Long-range gene regulation in hormone-dependent cancer.Nature reviews. Cancer · 2023Review
- ATAC-seq and RNA-seq analysis unravel the mechanism of sex differentiation and infertility in sex reversal chicken.Epigenetics & chromatin · 2023Article
- The interplay of sex steroid hormones and microRNAs in endometrial cancer: current understanding and future directions.Frontiers in endocrinology · 2023Review
- The Estrogen Receptor α Cistrome in Human Endometrium and Epithelial Organoids.Endocrinology · 2022Article
- Article
Corrections and comments
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Authors and funding
16 authors at 5 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Estrogen (E2) and Progesterone (Pg), via their specific receptors (ERalpha and PR), are major determinants in the development and progression of endometrial carcinomas, However, their precise mechanism of action and the role of other transcription factors involved are not entirely clear. Using Ishikawa endometrial cancer cells, we report that E2 treatment exposes a set of progestin-dependent PR binding sites which include both E2 and progestin target genes. ChIP-seq results from hormone-treated cells revealed a non-random distribution of PAX2 binding in the vicinity of these estrogen-promoted PR sites. Altered expression of hormone regulated genes in PAX2 knockdown cells suggests a role for PAX2 in fine-tuning ERalpha and PR interplay in transcriptional regulation. Analysis of long-range interactions by Hi-C coupled with ATAC-seq data showed that these regions, that we call 'progestin control regions' (PgCRs), exhibited an open chromatin state even before hormone exposure and were non-randomly associated with regulated genes. Nearly 20% of genes potentially influenced by PgCRs were found to be altered during progression of endometrial cancer. Our findings suggest that endometrial response to progestins in differentiated endometrial tumor cells results in part from binding of PR together with PAX2 to accessible chromatin regions. What maintains these regions open remains to be studied.
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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.