Transcriptome profile of RCS chondrocyte wt cell line and RCS chondrocyte obtained from a clone ko for the FGF receptors FGFR3 and FGFR4
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PROVIDER: PRJNA493251 | ENA |
REPOSITORIES: ENA
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Project description:To understand the transcriptomic effect of FGF18 treatment on Chondrocytes cells from wt rat and on Chondrocytes obtained from a clone ko for the FGF receptors FGFR3 and FGFR4, we performed Quant-seq experiments. Both cell lines were treated with Fibroblast growth factor 18 (FGF18), while untreated cells were used as control.
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Project description:Gene expression profiling of newborn lung tissue revealed few changes in compound FGFR3/FGFR4 deficient mice, consistent with their normal lung morphology at birth, suggesting the sequence of events leading to the phenotype initiates after birth in this model. Profiling of 4 week-old lung tissues revealed an induction of genes related to elastic fiber assembly in compound mutants. Lung RNA isolated from three animals of each genotype-age group were pooled for each Affymetrix chip (n=3 chips for each, except n=2 for wild type at 4 weeks.
2010-04-12 | E-GEOD-15452 | biostudies-arrayexpress
Project description:Gene expression profiling of newborn lung tissue revealed few changes in compound FGFR3/FGFR4 deficient mice, consistent with their normal lung morphology at birth, suggesting the sequence of events leading to the phenotype initiates after birth in this model. Profiling of 4 week-old lung tissues revealed an induction of genes related to elastic fiber assembly in compound mutants.
2010-03-31 | GSE15452 | GEO
Project description:To understand the determinants of chondrocyte FGF inhibitory response we sought to identify the unique set of proteins whose phosphorylation status is changed upon FGF treatment. RCS (Rat ChondroSarcoma) (RCS) cells were used for our experiments as a well-accepted model of proliferative chondrocytes which respond to FGF signaling with growth arrest Chondrocytes were treated with FGF1 and, as a control, cell cycle changes were monitored by FACScan analysis to demonstrate strong (around 95%) downregulation of S-phase at 24h. Three independent experiments were performed to obtain statistically representative datasets. We quantified 8299 proteins were quantified in the global proteome analysis using only unique or and razor peptides for quantitation . All proteins were identified in at least two replicates of a single treatment set by 2 or more peptides with 1% FDR Inclusion requirements for a single proteins were 1) two or more peptides identified with 51% FDR and 2) peptides that proteins were identified in at least 2 replicates of a single sample set.
2016-10-20 | MSV000080259 | MassIVE
Project description:Achondroplasia (ACH), the most common form of human dwarfism is caused by a mutation in the Fibroblast Growth Factor Receptor 3 (FGFR3) gene, resulting in constitutive activation of the receptor. In order to gain insight into molecular mechanisms involved in the physiopathology, a conditional mouse model carrying the Y367C mutation corresponding to the human Y373C TDI mutation was produced (fgfr3neoY367C/+). Crossing these mice with CMV-CRE mice produces dwarf fgfr3Y367C/+ and fgfr3+/+ controls littermates. Dwarf fgfr3Y367C/+ mice exhibited skeletal dysplasia at birth, the phenotype becoming progressively more pronounced as the mice got older, with reduced length of long bone, narrow trunk, short ribs and macrocephaly. Histological examination of epiphyseal growth plates showed a disorganized growth plate, with reduced size of the hypertrophic and proliferative zone and an accelerated secondary ossification center formation (full phenotype description in Pannier S et al, Activating Fgfr3 Y367C mutation causes hearing loss and inner ear defect in a mouse model of chondrodysplasia. Biochimica et biophysica acta 2009; Pannier S et al, Delayed bone age due to a dual effect of FGFR3 mutation in Achondroplasia. Bone 2010; Jonquoy A et al, A novel tyrosine kinase inhibitor restores chondrocyte differentiation and promotes bone growth in a gain-of-function Fgfr3 mouse model. Human molecular genetics 2012; Martin L et al, Constitutively-active FGFR3 disrupts primary cilium length and IFT20 trafficking in various chondrocyte models of achondroplasia. Human molecular genetics 2018).
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Project description:To better understand the molecular mechanisms underlying altered-FGFR3 oncogenic activity in bladder carcinomas, we made use of UMUC-14 cell lines, which endogenously expressed a mutated activated form of FGFR3 (FGFR3-S249C), the growth and transformation of these cell lines being dependent on activated-FGFR3 activity. We conducted a gene expression analysis using Affymetrix DNA arrays in this cell line treated or not with FGFR3 siRNAs.
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Project description:Rhabdomyosarcoma (RMS) is a paediatric cancer driven either by a fusion protein (e.g. PAX3-FOXO1) or by mutations in key signalling molecules (e.g. RAS or FGFR4). Despite the latter giving potential for precision medicine approaches in RMS, there are no such treatments implemented in the clinic yet. In order to identify and test novel precision therapy strategies, appropriate cellular and mouse models are crucial. We have here thoroughly characterized a RMS patient-derived cell line model, RMS559, which harbours a FGFR4 V550L activating mutation with high allelic frequency (0.8). Importantly, we show that RMS559 cells are oncogenically dependent on FGFR4 signalling by treatment with the pan-FGFR inhibitor LY2874455. Phosphoproteomic analysis identified RAS/MAPK and PI3K/AKT as the major druggable signalling pathways downstream of FGFR V550L. Inhibitors against these pathways inhibited cell proliferation. Furthermore, we found that FGFR4 V550L is dependent on HSP90 and inhibitors targeting HSP90 efficiently restrain proliferation. Recently, FGFR4 specific inhibitors have been developed. While two of these, BLU-9931 and H3B-6527, did not efficiently inhibit FGFR4 V550L, probably because of the gatekeeper mutation (V550L), one of them, FGF401 inhibited FGFR4 V550L and cell proliferation at low nanomolar concentrations. Finally, we developed a mouse model using RMS559 cells and tested the in vivo efficacy of LY2874455 and FGF401. While LY2874455 inefficiently inhibited growth, FGF401 completely abrogated tumour growth in vivo.
2022-10-19 | PXD029719 | Pride
Project description:To better understand the molecular mechanisms underlying altered-FGFR3 oncogenic activity in bladder carcinomas, we made use of MGH-U3 cell lines, which were derived from a human bladder tumor and endogenously expressed a mutated activated form of FGFR3 (FGFR3-Y375C), the growth and transformation of these cell lines being dependent on activated-FGFR3 activity. We conducted a gene expression analysis using Affymetrix DNA arrays in this cell line treated or not with FGFR3 siRNAs.
2018-02-16 | GSE84731 | GEO
Project description:To better understand the molecular mechanisms underlying altered-FGFR3 oncogenic activity in bladder carcinomas, we made use of RT112 cell lines, which were derived from a human bladder tumor and endogenously expressed the FGFR3-TACC3 fusion protein, the growth and transformation of these cell lines being dependent on activated-FGFR3 activity. We conducted a gene expression analysis using Affymetrix DNA arrays in this cell line treated or not with FGFR3 siRNAs.
2018-02-16 | GSE84732 | GEO
