ArticleScientific reports2015
In PC3 prostate cancer cells ephrin receptors crosstalk to β1-integrins to strengthen adhesion to collagen type I.
Article in Scientific reports, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 20 citations in OpenAlex.
- Homotypic Targeting of [Pharmaceutics · 2025Article
- A Pharmacological Investigation of Eph-Ephrin Antagonism in Prostate Cancer: UniPR1331 Efficacy Evidence.Pharmaceuticals (Basel, Switzerland) · 2023Article
- Host deficiency in ephrin-A1 inhibits breast cancer metastasis.F1000Research · 2020Article
- Article
- Blood vessels guide Schwann cell migration in the adult demyelinated CNS through Eph/ephrin signaling.Acta neuropathologica · 2019Article
- Article
- The osteoprogenitor-specific loss of ephrinB1 results in an osteoporotic phenotype affecting the balance between bone formation and resorption.Scientific reports · 2018Article
- αV-class integrins exert dual roles on α5β1 integrins to strengthen adhesion to fibronectin.Nature communications · 2017Article
- Dynamic interplay between adhesion surfaces in carcinomas: Cell-cell and cell-matrix crosstalk.World journal of biological chemistry · 2016Review
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Authors and funding
4 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Eph receptor (Eph) and ephrin signaling can play central roles in prostate cancer and other cancer types. Exposed to ephrin-A1 PC3 prostate cancer cells alter adhesion to extracellular matrix (ECM) proteins. However, whether PC3 cells increase or reduce adhesion, and by which mechanisms they change adhesion to the ECM remains to be characterized. Here, we assay how ephrin-A1 stimulates PC3 cells to adhere to ECM proteins using single-cell force spectroscopy. We find that PC3 cells binding to immobilized ephrin-A1 but not to solubilized ephrin-A1 specifically strengthen adhesion to collagen I. This Eph-ephrin-A1 signaling, which we suppose is based on mechanotransduction, stimulates β1-subunit containing integrin adhesion via the protein kinase Akt and the guanine nucleotide-exchange factor cytohesin. Inhibiting the small GTPases, Rap1 or Rac1, generally lowered adhesion of PC3 prostate cancer cells. Our finding suggests a mechanism by which PC3 prostate cancer cells exposed to ephrins crosstalk to β1-integrins and preferably metastasize in bone, a collagen I rich tissue.
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