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Alterations in Cell Growth and Signaling in ErbB3 Binding Protein -1 (Ebp1) Deficient Mice

ABSTRACT: Background: The ErbB3 binding protein-1 (Ebp1) belongs to a family of DNA/RNA binding proteins implicated in cell growth, apoptosis and differentiation. However, the physiological role of Ebp1 in the whole organism is not known. Therefore, we generated Ebp1-deficient mice carrying a gene trap insertion in intron 2 of the Ebp1 (pa2g4) gene. Results: Ebp1 -/- mice were on average 30% smaller than wild type and heterozygous sex matched littermates. Growth retardation was apparent from Day 10 until Day 30. IGF-1 production and IGBP-3 and 4 protein levels were reduced in both embryo fibroblasts and adult knock-out mice. The proliferation of fibroblasts derived from Day 12.5 knock out embryos was also decreased as compared to that of wild type cells. Microarray expression analysis revealed changes in genes important in cell growth including members of the MAPK signal transduction pathway. In addition, the expression or activation of proliferation related genes such as AKT and the androgen receptor, previously demonstrated to be affected by Ebp1 expression in vitro, were altered in adult tissues. Conclusions: These results indicate that Ebp1 can affect growth in an animal model, but that the expression of proliferation related genes is cell and context specific. The Ebp1-/- mouse line represents a new in vivo model to investigate Ebp1 function in the whole organism.

ORGANISM(S): Mus musculus

PROVIDER: GSE13718 | GEO | 2009/03/31

SECONDARY ACCESSION(S): PRJNA110395

REPOSITORIES: GEO

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Alterations in Cell Growth and Signaling in ErbB3 Binding Protein -1 (Ebp1) Deficient Mice

Project description:Background: The ErbB3 binding protein-1 (Ebp1) belongs to a family of DNA/RNA binding proteins implicated in cell growth, apoptosis and differentiation. However, the physiological role of Ebp1 in the whole organism is not known. Therefore, we generated Ebp1-deficient mice carrying a gene trap insertion in intron 2 of the Ebp1 (pa2g4) gene. Results: Ebp1 -/- mice were on average 30% smaller than wild type and heterozygous sex matched littermates. Growth retardation was apparent from Day 10 until Day 30. IGF-1 production and IGBP-3 and 4 protein levels were reduced in both embryo fibroblasts and adult knock-out mice. The proliferation of fibroblasts derived from Day 12.5 knock out embryos was also decreased as compared to that of wild type cells. Microarray expression analysis revealed changes in genes important in cell growth including members of the MAPK signal transduction pathway. In addition, the expression or activation of proliferation related genes such as AKT and the androgen receptor, previously demonstrated to be affected by Ebp1 expression in vitro, were altered in adult tissues. Conclusions: These results indicate that Ebp1 can affect growth in an animal model, but that the expression of proliferation related genes is cell and context specific. The Ebp1-/- mouse line represents a new in vivo model to investigate Ebp1 function in the whole organism. Isolation of Mouse Embryo Fibroblasts (MEFS) and proliferation assays. Embryos (12.5 days) were minced and incubated in 0.25% trypsin and 5 U of DNAse I for 37º C for 30 min. Dulbecco’s MEM supplemented with 10% fetal bovine serum and penicillin and streptomycin were added to the cell suspension and cells centrifuged at 1000 rpm for 10 min. The pellet was resuspended in medium and cells were grown in MEM and passaged by trypsinization.

2009-03-31 | E-GEOD-13718 | biostudies-arrayexpress

RNA-Seq analysis of total mouse neocortex during development

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Ebp1-selective ribosome profiling analysis of Neuro2a cells with Ebp1-immuno-precipitation

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Ribosome profiling analysis of Neuro2a cells with Ebp1 knockdown

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Ebp1-selective ribosome profiling analysis of Neuro2a cells with Ebp1-immuno-precipitation

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Transcription profiling of human prostate cancer cell line to determine Ebp1 effect in prostate cancer

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Protein synthesis in the developing neocortex at near-atomic resolution reveals Ebp1-mediated neuronal proteostasis at the 60S tunnel exit

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Protein synthesis in the developing neocortex at near-atomic resolution reveals Ebp1-mediated neuronal proteostasis at the 60S tunnel exit

2021-01-04 | PXD014841 | Pride

The ErbB3-binding protein EBP1 modulates lapatinib sensitivity in prostate cancer cells.

Project description:Although ErbB receptors have been implicated in prostate cancer progression, ErbB-directed drugs have not proven effective for prostate cancer treatment. The ErbB3-binding protein EBP1 affects both ErbB2 and androgen receptor signaling, two components of the response to ErbB-targeted therapies. We therefore examined the effects of EBP1 expression on the response to the ErbB1/2 tyrosine kinase inhibitor lapatinib. We found a negative correlation between endogenous EBP1 levels and lapatinib sensitivity in prostate cancer cell lines. We then overexpressed or inhibited expression of EBP1. Silencing EBP1 expression increased lapatinib sensitivity and overexpression of EBP1 increased resistance in androgen-containing media. Androgen depletion resulted in an increased sensitivity of androgen-dependent EBP1 expressing cells to lapatinib, but did not affect the lapatinib sensitivity of hormone resistant cells. However, EBP1 silenced cells were still more sensitive to lapatinib than EBP1-expressing cells in the absence of androgens. The increase in sensitivity to lapatinib following EBP1 silencing was associated with increased ErbB2 levels. In addition, lapatinib treatment increased ErbB2 levels in sensitive cells that express low levels of EBP1, but decreased ErbB2 levels in resistant EBP1-expressing cells. In contrast, ErbB3 and phospho ErbB3 levels were not affected by either changes in EBP1 levels or lapatinib treatment. The production of the ErbB3/4 ligand heregulin was increased in EBP1-silenced cells. EBP1-induced changes in AR levels were not associated with changes in lapatinib sensitivity. These studies suggest that the ability of EBP1 to activate ErbB2 signaling pathways results in increased lapatinib sensitivity.

| S-EPMC4449279 | biostudies-literature

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