ArticleEndocrinology2010
Estrogen stimulation of cell migration involves multiple signaling pathway interactions.
Article in Endocrinology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 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.
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
29 citing papers in PubMed, 69 citations in OpenAlex.
- Steroidogenic Acute Regulatory Protein in Breast Cancer: Mechanistic Insights into Pathogenesis and Therapeutics.International journal of molecular sciences · 2026Review
- Paxillin and Kindlin: Research Progress and Biological Functions.Biomolecules · 2025Review
- G protein-coupled estrogen receptor expression in postnatal developing mouse retina.Frontiers in ophthalmology · 2024Article
- Estrogen Receptor Signaling in Breast Cancer.Cancers · 2023Review
- 17-β Estradiol up-regulates energy metabolic pathways, cellular proliferation and tumor invasiveness in ER+ breast cancer spheroids.Frontiers in oncology · 2022Article
- Combinatorial treatments of tamoxifen and SM6Met, an extract fromFrontiers in pharmacology · 2022Article
- Estrogens and the regulation of glucose metabolism.World journal of diabetes · 2021Review
- Long-term exposure to triclosan increases migration and invasion of human breast epithelial cells in vitro.Journal of applied toxicology : JAT · 2021Article
- Heregulin-induced cell migration is prevented by trastuzumab and trastuzumab-emtansine in HER2+ breast cancer.Breast cancer research and treatment · 2021Article
- Screening and Identification of Novel Potential Biomarkers for Breast Cancer Brain Metastases.Frontiers in oncology · 2021Article
- The Cell-Free Expression of MiR200 Family Members Correlates with Estrogen Sensitivity in Human Epithelial Ovarian Cells.International journal of molecular sciences · 2020Article
- Focus on the glycerophosphocholine pathway in choline phospholipid metabolism of cancer.NMR in biomedicine · 2019Review
- Estrogen receptor signaling mechanisms.Advances in protein chemistry and structural biology · 2019Review
- Extranuclear signaling by sex steroid receptors and clinical implications in breast cancer.Molecular and cellular endocrinology · 2018Review
- Intracellular IL-37b interacts with Smad3 to suppress multiple signaling pathways and the metastatic phenotype of tumor cells.Oncogene · 2017Article
- Article
- Alternatively spliced tissue factor synergizes with the estrogen receptor pathway in promoting breast cancer progression.Journal of thrombosis and haemostasis : JTH · 2015Article
- Overlapping nongenomic and genomic actions of thyroid hormone and steroids.Best practice & research. Clinical endocrinology & metabolism · 2015Review
- Identification of Estrogen Response Element in Aquaporin-3 Gene that Mediates Estrogen-induced Cell Migration and Invasion in Estrogen Receptor-positive Breast Cancer.Scientific reports · 2015Article
- Transcriptome analysis of cattle muscle identifies potential markers for skeletal muscle growth rate and major cell types.BMC genomics · 2015Article
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 3 countries.
Funding
Abstract
Hormone-dependent breast cancers respond to inhibitors of estrogen synthesis or action with tumor regression and with a reduction of new metastases. The mechanisms underlying the effects of estrogen on metastasis likely differ from those on tumor regression. Cell migration is a key first step in the metastatic process. Based on our prior work and other published data, we designed and tested a working model that suggested that estrogen receptor α, epidermal growth factor receptor, focal adhesion kinase (FAK), paxillin, phosphatidylinositol 3 kinase, p60 Src tyrosine kinase (c-Src), c-Jun N-terminal kinase, and MAPK interact to facilitate estradiol (E(2))-induced cell migration. Accordingly, we examined the effect of E(2) on activation of these pathways and demonstrated mechanistic effects by blocking each component and assessing cell migration as a biologic endpoint. Initial studies validated a robust cell migration assay characterized by highly reproducible, dose-dependent responses to E(2). Examining various mechanisms involved in migration, we showed that E(2) induced activation of c-Src, FAK, and paxillin with early peaks within 5-30 min and later peaks at 24 h. ERK and protein kinase B phosphorylation exhibited only early peaks. Blockade of various steps in these signaling pathways with use of small interfering RNA or specific inhibitors demonstrated mechanistic effects of these signaling molecules on cell migration. Our results suggest that the effects of E(2) on cell migration involve multiple, interacting signaling pathways. Important effects are mediated by the MAPK, phosphatidylinositol 3 kinase, and c-Jun N-terminal kinase pathways and use FAK, paxillin, and c-Src for activation. Each pathway represents a potential target for blocking cell migration and metastasis of breast cancer 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.