ArticleJournal of biochemical and molecular toxicology2025
Estrogen Promotes the Proliferation and Migration of Endometrial Cancer Through the GPER-Mediated NOTCH Pathway.
Article in Journal of biochemical and molecular toxicology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
What it found
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The trial behind it
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Who cites it
5 citing papers in PubMed.
- Estradiol Promotes Tumor Progression in ERα-Low Endometrial Cancer via the GPER/SphK1 Pathway.Journal of biochemical and molecular toxicology · 2026Article
- Natural Products in Endometrial Cancer: Molecular Mechanisms, Preclinical Evidence, and Clinical Perspectives.Current issues in molecular biology · 2026Review
- Sex hormone receptor signaling networks drive pancreatic solid-pseudopapillary neoplasm pathogenesis and therapy.Discover oncology · 2025Review
- GPER in metabolic homeostasis and disease: molecular mechanisms, nutritional regulation, and therapeutic potential.Journal of translational medicine · 2025Review
- NF-κB as an Inflammatory Biomarker in Thin Endometrium: Predictive Value for Live Birth in Recurrent Implantation Failure.Diagnostics (Basel, Switzerland) · 2025Article
Corrections and comments
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Authors and funding
8 authors.
Funding
Abstract
This study aims to investigate the expression of GPER in EC, assess the impact of estrogen on the proliferation and migration of EC via GPER, and examine the potential role of GPER in mediating the NOTCH pathway to influence EC proliferation and migration. The expression of GPER and its correlation with clinicopathological features were investigated using clinical data. Cell proliferation was assessed through MTT and EdU assays, while cell migration ability was evaluated using wound healing and transwell assays. Western blot analysis was conducted to detect proteins associated with the GPER and NOTCH signaling pathways. Additionally, xenograft tumor models were established to investigate the potential role of estrogen in mediating the NOTCH pathway via GPER. The results demonstrated a significant upregulation of GPER expression in EC, which was associated with clinical stage and metastasis. In vitro experiments provided evidence that estrogen promotes EC cell proliferation and metastasis by enhancing the expression levels of GPER, Notch1, and Hes-1 proteins. Conversely, knocking down or suppressing GPER effectively reverses these effects. Furthermore, treatment with JAG-1, an agonist for the NOTCH pathway, counteracts si-GPER's inhibitory impact on both proliferation and migration abilities of EC cells while increasing Notch1 and Hes-1 protein expression levels; however, it does not alter GPER expression. In vivo experiments have substantiated that estrogen facilitates EC proliferation via the GPER-mediated NOTCH pathway.
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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.