ArticleReproductive biology and endocrinology : RB&E2009
Genes targeted by the estrogen and progesterone receptors in the human endometrial cell lines HEC1A and RL95-2.
Article in Reproductive biology and endocrinology : RB&E, 2009. 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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Who cites it
12 citing papers in PubMed, 26 citations in OpenAlex.
- Knockdown of CTMP Enhances Progesterone Sensitivity in Endometrial Cancer by Inhibiting the PI3K/AKT Signaling Pathway.Reproductive sciences (Thousand Oaks, Calif.) · 2025Article
- Regulation of RNA splicing in endometrial tissue and its association with endometriosis.iScience · 2025Article
- Atlas-scale metabolic activities inferred from single-cell and spatial transcriptomics.bioRxiv : the preprint server for biology · 2025Article
- Estetrol Increases Progesterone Genetic Response without Triggering Common Estrogenic Effects in Endometriotic Cell Lines and Primary Cultures.Biomedicines · 2023Article
- Fractalkine Regulates HEC-1A/JEG-3 Interaction by Influencing the Expression of Implantation-Related Genes in an In Vitro Co-Culture Model.International journal of molecular sciences · 2020Article
- Human Endometrial Transcriptome and Progesterone Receptor Cistrome Reveal Important Pathways and Epithelial Regulators.The Journal of clinical endocrinology and metabolism · 2020Article
- Transcriptomic analysis of the interaction of choriocarcinoma spheroids with receptive vs. non-receptive endometrial epithelium cell lines: an in vitro model for human implantation.Journal of assisted reproduction and genetics · 2019Article
- Detecting Differential Transcription Factor Activity from ATAC-Seq Data.Molecules (Basel, Switzerland) · 2018Article
- The regulation of Hh/Gli1 signaling cascade involves Gsk3β- mediated mechanism in estrogen-derived endometrial hyperplasia.Scientific reports · 2017Article
- Progesterone receptor transcriptome and cistrome in decidualized human endometrial stromal cells.Endocrinology · 2015Article
- The Epigenetics of Normal Pregnancy.Obstetric medicine · 2013Review
- Extracellular signal-regulated kinase 1/2 signaling pathway is required for endometrial decidualization in mice and human.PloS one · 2013Article
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundWhen the steroid hormones estrogen and progesterone bind to nuclear receptors, they have transcriptional impact on target genes in the human endometrium. These transcriptional changes have a critical function in preparing the endometrium for embryo implantation.
methods382 genes were selected, differentially expressed in the receptive endometrium, to study their responsiveness of estrogen and progesterone. The endometrial cell lines HEC1A and RL95-2 were used as experimental models for the non-receptive and receptive endometrium, respectively. Putative targets for activated steroid hormone receptors were investigated by chromatin immunoprecipitation (ChIP) using receptor-specific antibodies. Promoter occupancy of the selected genes by steroid receptors was detected in ChIP-purified DNA by quantitative PCR (qPCR). Expression analysis by reverse transcriptase (RT)-PCR was used to further investigate hormone dependent mRNA expression regulation of a subset of genes.
resultsChIP-qPCR analysis demonstrated that each steroid hormone receptor had distinct group of target genes in the endometrial cell lines. After estradiol treatment, expression of estrogen receptor target genes predominated in HEC1A cells (n = 137) compared to RL95-2 cells (n = 35). In contrast, expression of progesterone receptor target genes was higher in RL95-2 cells (n = 83) than in HEC1A cells (n = 7) after progesterone treatment. RT-PCR analysis of 20 genes demonstrated transcriptional changes after estradiol or progesterone treatment of the cell lines.
conclusionsCombined results from ChIP-qPCR and RT-PCR analysis showed different patterns of steroid hormone receptor occupancy at target genes, corresponding to activation or suppression of gene expression after hormone treatment of HEC1A and RL95-2 cell lines.
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