ArticleCells2020
Estradiol Induces Epithelial to Mesenchymal Transition of Human Glioblastoma Cells.
Article in Cells, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.
What it found
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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.
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.
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Who cites it
35 citing papers in PubMed, 40 citations in OpenAlex.
- G protein-coupled estrogen receptor (GPER) modulates epithelial-mesenchymal transition-like phenotype in human glioblastoma cells.Cell adhesion & migration · 2026Article
- Involvement of claudins 6 and 9 in epithelial-mesenchymal transition and the metastatic process.Tissue barriers · 2026Review
- The significance of epithelial-mesenchymal transition (EMT) in the initiation, plasticity, and treatment of glioblastoma.Genes & diseases · 2026Review
- Evaluation of (Z)-endoxifen as a potential therapy for glioblastoma multiforme through computational and experimental analyses.Scientific reports · 2025Article
- Intranasal AβJournal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2025Article
- Transcriptomic-Driven Drug Repurposing Reveals SP600125 as a Promising Drug Candidate for the Treatment of Glial-Mesenchymal Transition in Glioblastoma.International journal of molecular sciences · 2025Article
- Knockdown of ACC1 promotes migration and invasion of U251 glioma cells by epigenetically suppressing SDH.International journal of oncology · 2025Article
- Fast Evolving Glioblastoma in a Pregnant Woman: Diagnostic and Therapeutic Challenges.Diagnostics (Basel, Switzerland) · 2025Article
- Sesquiterpene Lactones as Promising Anti-Glioblastoma Drug Candidates Exerting Complex Effects on Glioblastoma Cell Viability and Proneural-Mesenchymal Transition.Biomedicines · 2025Review
- Neurosteroids in Glioma: A Novel Therapeutic Concept.Life (Basel, Switzerland) · 2024Review
- Comprehensive understanding of glioblastoma molecular phenotypes: classification, characteristics, and transition.Cancer biology & medicine · 2024Review
- High core 1β1,3-galactosyltransferase 1 expression is associated with poor prognosis and promotes cellular radioresistance in lung adenocarcinoma.Journal of cancer research and clinical oncology · 2024Article
- Estrogen α and β Receptor Expression in the Various Regions of Resected Glioblastoma Multiforme Tumors and in an In Vitro Model.International journal of molecular sciences · 2024Article
- A Review of Approaches to Potentiate the Activity of Temozolomide against Glioblastoma to Overcome Resistance.International journal of molecular sciences · 2024Review
- Article
- Exploring the potential of tamoxifen-based copper(ii) dichloride in breast cancer therapy.RSC medicinal chemistry · 2023Article
- Estradiol-Induced Epithelial to Mesenchymal Transition and Migration Are Inhibited by Blocking c-Src Kinase in Breast Cancer Cell Lines.Journal of breast cancer · 2023Article
- Glioblastoma in pregnant patient with pathologic and exogenous sex hormone exposure and family history of high-grade glioma: A case report and review of the literature.Surgical neurology international · 2023Article
- Expression and estrogen regulation of G protein-coupled estrogen receptor in human glioblastoma cells.Oncology letters · 2022Article
- Evolution of 3-(4-hydroxyphenyl)indoline-2-one as a scaffold for potent and selective anticancer activity.RSC medicinal chemistry · 2022Review
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The mesenchymal phenotype of glioblastoma multiforme (GBM), the most frequent and malignant brain tumor, is associated with the worst prognosis. The epithelial-mesenchymal transition (EMT) is a cell plasticity mechanism involved in GBM malignancy. In this study, we determined 17β-estradiol (E2)-induced EMT by changes in cell morphology, expression of EMT markers, and cell migration and invasion assays in human GBM-derived cell lines. E2 (10 nM) modified the shape and size of GBM cells due to a reorganization of actin filaments. We evaluated EMT markers expression by RT-qPCR, Western blot, and immunofluorescence.We found that E2 upregulated the expression of the mesenchymal markers, vimentin, and N-cadherin. Scratch and transwell assays showed that E2 increased migration and invasion of GBM cells. The estrogen receptor-α (ER-α)-selective agonist 4,4',4''-(4-propyl-[1H]-pyrazole-1,3,5-triyl)trisphenol (PPT, 10 nM) affected similarly to E2 in terms of the expression of EMT markers and cell migration, and the treatment with the ER-α antagonist methyl-piperidino-pyrazole (MPP, 1 μM) blocked E2 and PPT effects. ER-β-selective agonist diarylpropionitrile (DNP, 10 nM) and antagonist 4-[2-phenyl-5,7-bis(trifluoromethyl)pyrazole[1,5-a]pyrimidin-3-yl]phenol (PHTPP, 1 μM) showed no effects on EMT marker expression. These data suggest that E2 induces EMT activation through ER-α in human GBM-derived cells.
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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.