ArticleProceedings of the National Academy of Sciences of the United States of America1997
Trans receptor inhibition of human glioblastoma cells by erbB family ectodomains.
Article in Proceedings of the National Academy of Sciences of the United States of America, 1997. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 54 citations in OpenAlex.
- Functional EGF domain of the human neuregulin 1α produced in Escherichia coli with accurate disulfide bonds.Molecular biology reports · 2022Article
- Novel vaccines for glioblastoma: clinical update and perspective.Immunotherapy · 2016Review
- Disabling of the erbB Pathway Followed by IFN-γ Modifies Phenotype and Enhances Genotoxic Eradication of Breast Tumors.Cell reports · 2015Article
- Reversion of the ErbB malignant phenotype and the DNA damage response.Experimental and molecular pathology · 2012Review
- Targeting erbB receptors.Seminars in cell & developmental biology · 2010Review
- Virtual prototyping study shows increased ATPase activity of Hsp90 to be the key determinant of cancer phenotype.Systems and synthetic biology · 2010Article
- EGFR Intron Recombination in Human Gliomas: Inappropriate Diversion of V(D)J Recombination?Current genomics · 2007Article
- Distinct domains in the SHP-2 phosphatase differentially regulate epidermal growth factor receptor/NF-kappaB activation through Gab1 in glioblastoma cells.Molecular and cellular biology · 2004Article
- Article
- Activation of STAT5 triggers proliferation and contributes to anti-apoptotic signalling mediated by the oncogenic Xmrk kinase.Oncogene · 2002Article
- CD95-mediated apoptosis of human glioma cells: modulation by epidermal growth factor receptor activity.Brain pathology (Zurich, Switzerland) · 2002Article
- The tyrosine phosphatase SHP-2 is required for mediating phosphatidylinositol 3-kinase/Akt activation by growth factors.Oncogene · 2001Article
- Article
- The role of distinct p185neu extracellular subdomains for dimerization with the epidermal growth factor (EGF) receptor and EGF-mediated signaling.Proceedings of the National Academy of Sciences of the United States of America · 2001Article
- Regulation of CD40 function by its isoforms generated through alternative splicing.Proceedings of the National Academy of Sciences of the United States of America · 2001Article
- HER2/neu: mechanisms of dimerization/oligomerization.Oncogene · 2000Review
- Article
- Oncogenic epidermal growth factor receptor mutants with tandem duplication: gene structure and effects on receptor function.Oncogene · 2000Article
- The HER-2/neu receptor tyrosine kinase gene encodes a secreted autoinhibitor.Proceedings of the National Academy of Sciences of the United States of America · 1999Article
- Induction of the Tat-binding protein 1 gene accompanies the disabling of oncogenic erbB receptor tyrosine kinases.Proceedings of the National Academy of Sciences of the United States of America · 1999Article
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Our aim has been to understand the features of erbB receptor homo- and heterodimer assembly to develop approaches to disrupt receptor activation. We have developed a general approach to cause erbB receptor-specific trans inhibition of human neoplasia. The clonal progression of human astrocytomas to a more malignant phenotype often involves the amplification and overexpression of the epidermal growth factor receptor (EGFr) gene. We have selectively targeted the EGFr in human glioblastoma cells with kinase-deficient mutants of the erbB family derived from the ectodomain of the Neu oncogene that are able to form heterodimers with EGFr and inhibit EGFr-dependent phenotypes. In EGFr-positive U87MG human glioblastoma cells, expression of the Neu ectodomain inhibits EGF-, but not platelet-derived growth factor-, induced DNA synthesis; inhibits cell proliferation in the presence of EGF, but not platelet-derived growth factor; inhibits the ability of U87MG to form colonies in soft agar; and inhibits transforming efficiency in athymic mice. These studies establish that EGFr-mediated signal transduction is important in the maintenance of malignant glioma, and that trans receptor inhibition is a novel way to abrogate abnormal growth of these tumors. Neu ectodomains will be useful in determining the manner in which the EGFr contributes to glial tumorigenesis and in the design of pharmaceuticals that disable erbB family oncoproteins. In addition, these studies provide a rationale for the application of the Neu ectodomain in gene therapy approaches to human malignant glioma and, potentially, to other systemic epithelial malignancies expressing erbB family receptors.
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