ArticleScientific reports2015
EphB2 activation is required for ependymoma development as well as inhibits differentiation and promotes proliferation of the transformed cell.
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 13 papers.
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Who cites it
13 citing papers in PubMed, 14 citations in OpenAlex.
- Targeting EPHB2/ABL1 restores antitumor immunity in preclinical models of ependymoma.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Beyond cell-cell contact: therapeutic potential of Eph signaling in central nervous system tumors.Frontiers in molecular neuroscience · 2025Review
- The Clinical Relevance of the EPH/Ephrin Signaling Pathway in Pediatric Solid and Hematologic Malignancies.International journal of molecular sciences · 2024Review
- PRMT5 inhibition shows in vitro efficacy against H3K27M-altered diffuse midline glioma, but does not extend survival in vivo.Scientific reports · 2024Article
- The biology of ependymomas and emerging novel therapies.Nature reviews. Cancer · 2022Review
- Review
- Review
- Loss of tyrosine kinase receptor Ephb2 impairs proliferation and stem cell activity of spermatogonia in culture†.Biology of reproduction · 2020Article
- Periodic acid‑Schiff staining method for function detection of liver cells is affected by 2% horse serum in induction medium.Molecular medicine reports · 2017Article
- Transcriptional Dependencies in Diffuse Intrinsic Pontine Glioma.Cancer cell · 2017Article
- Combined EphB2 receptor knockdown with radiation decreases cell viability and invasion in medulloblastoma.Cancer cell international · 2017Article
- Translating preclinical hopes into clinical reality for children with ependymoma.Neuro-oncology · 2015Article
- Stimulation of EphB2 attenuates tau phosphorylation through PI3K/Akt-mediated inactivation of glycogen synthase kinase-3β.Scientific reports · 2015Article
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
Our intracranial implantation mouse model of ependymoma clearly demonstrates overexpression of the ephrin receptor EphB2 in Ink4a/Arf((-/-)) supratentorial embryonic neural stem cells (STeNSCs) to be essential for transformation and disease development; however the requirement for and consequence of receptor activation on transformation and neural stem cell function were not examined. We definitively illustrate the necessity for receptor activation in cellular transformation and the importance of implantation site and microenvironment in directing ependymoma development. In vitro assays of EphB2 overexpressing Ink4a/Arf((-/-)) STeNSCs showed no changes in their neural stem cell characteristics (stem cell marker expression and self-renewal) upon receptor activation, but EphB2 driven tumor cells were inhibited significantly in differentiation and exhibited increased tumorsphere formation and cellular proliferation in response to ephrin-B ligand mediated receptor activation. Additionally, we observed substantial differences in the phosphorylation state of several key proteins involved in Ras and p38 MAPK signaling when comparing EphB2 overexpressing Ink4a/Arf((-/-)) STeNSCs and tumor cells with relatively little change in total protein levels. We propose that EphB2 mediated ependymoma development is a multifactorial process requiring microenvironment directed receptor activation, resulting in changes in the phosphorylation status of key regulatory proteins, maintenance of a stem-like state and cellular proliferation.
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