ArticleCells2022
SWI/SNF Antagonism of PRC2 Mediates Estrogen-Induced Progesterone Receptor Expression.
Article in Cells, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
19 citing papers in PubMed, 22 citations in OpenAlex.
- From Epigenetic Dysregulation to Therapeutic Reprogramming in Endometrial Cancer: A State-Response Framework for Treatment Resistance.International journal of molecular sciences · 2026Review
- esBAF and INO80C fine-tune subcompartments and differentially regulate enhancer-promoter interactions.Genetics · 2026Article
- Does immunotherapy hold great promise in endometrial cancer care?Frontiers in immunology · 2026Review
- Multidimensional OMICs reveal ARID1A orchestrated control of DNA damage, splicing, and cell cycle in normal-like and malignant urothelial cells.Molecular oncology · 2025Article
- esBAF and INO80C fine-tune subcompartments and differentially regulate enhancer-promoter interactions.bioRxiv : the preprint server for biology · 2025Article
- ARID1A: gene, protein, and function in endometrial cancer.Oncogene · 2025Review
- Advances in the molecular mechanisms underlying progestin resistance in endometrial cancer.Fundamental research · 2025Review
- Article
- Review
- Genome-Wide CRISPR Screen Identifies KEAP1 Perturbation as a Vulnerability of ARID1A-Deficient Cells.Cancers · 2024Article
- Estrogen Receptor (ER) and Progesterone Receptor (PgR) Expression in Endometrial Cancer-An Immunohistochemical Assessment.Diagnostics (Basel, Switzerland) · 2024Article
- Review
- Explore the alterations of downstream molecular pathways caused by ARID1A mutation/knockout in human endometrial cancer cells.Journal of cancer research and clinical oncology · 2023Article
- PIK3CA mutation in endometriotic epithelial cells promotes viperin-dependent inflammatory response to insulin.Reproductive biology and endocrinology : RB&E · 2023Article
- Targeting the mevalonate pathway suppresses ARID1A-inactivated cancers by promoting pyroptosis.Cancer cell · 2023Article
- The interplay of sex steroid hormones and microRNAs in endometrial cancer: current understanding and future directions.Frontiers in endocrinology · 2023Review
- Progestin Resistance and Corresponding Management of Abnormal Endometrial Hyperplasia and Endometrial Carcinoma.Cancers · 2022Review
- AP-1 Subunit JUNB Promotes Invasive Phenotypes in Endometriosis.Reproductive sciences (Thousand Oaks, Calif.) · 2022Article
- Enhancing progestin therapy via HDAC inhibitors in endometrial cancer.American journal of cancer research · 2022Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 3 institutions in 1 country.
Funding
Abstract
Endometrial cancer (EC) is characterized by high estrogen levels unopposed by progesterone. Treatment with progestins is standard for early EC, but the response to progestins is dependent on progesterone receptor (PGR) expression. Here, we show that the expression of PGR in endometrial epithelial cells is dependent on ARID1A, a DNA-binding subunit of the SWI/SNF chromatin-remodeling complex that is commonly mutated in EC. In endometrial epithelial cells with estrogen receptor overexpression, we find that ARID1A promotes estrogen signaling and regulates common gene expression programs. Normally, endometrial epithelial cells expressing estrogen receptors respond to estrogen by upregulating the PGR. However, when ARID1A expression is lost, upregulation of PGR expression is significantly reduced. This phenomenon can also occur following the loss of the SWI/SNF subunit BRG1, suggesting a role for ARID1A- and BRG1-containing complexes in PGR regulation. We find that PGR is regulated by a bivalent promoter, which harbors both H3K4me3 and H3K27me3 histone tail modifications. H3K27me3 is deposited by EZH2, and inhibition of EZH2 in the context of ARID1A loss results in restoration of estrogen-induced PGR expression. Our results suggest a role for ARID1A deficiency in the loss of PGR in late-stage EC and a therapeutic utility for EZH2 inhibitors in this disease.
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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.