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Transcriptome profile of RCS chondrocyte wt cell line and RCS chondrocyte obtained from a clone ko for the FGF receptors FGFR3 and FGFR4

ABSTRACT: 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.

ORGANISM(S): Rattus norvegicus

PROVIDER: GSE120516 | GEO | 2020/07/13

REPOSITORIES: GEO

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Transcriptome profile of RCS chondrocyte wt cell line and RCS chondrocyte obtained from a clone ko for the FGF receptors FGFR3 and FGFR4

Project description:Transcriptome profile of RCS chondrocyte wt cell line and RCS chondrocyte obtained from a clone ko for the FGF receptors FGFR3 and FGFR4

| PRJNA493251 | ENA

Expression data from lung of mice bearing mutations of FGFR3 and FGFR4

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

Expression data from lung of mice bearing mutations of FGFR3 and FGFR4

2010-03-31 | GSE15452 | GEO

Gene expression data from UMUC-14 following FGFR3 knock-down using FGFR3 siRNAs

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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Strategies to inhibit FGFR4 V550L-driven rhabdomyosarcoma

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

Gene expression data from MGH-U3 following FGFR3 knock-down using FGFR3 siRNAs

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.

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Gene expression data from RT112 following FGFR3 knock-down using FGFR3 siRNAs

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

FGFR3 knock-down

Project description:FGFR3 knock-down

| PRJNA330963 | ENA

Profibrotic regulation of FGFR3 signaling in fibroblasts

Project description:We employed dermal fibroblasts isolated from Fgfr3G374Rneo+ mice, which do not express functional Fgfr3 (Fgfr3KO), from Fgfr3G374Rneo- mice with ligand-independent constitutive activation of Fgfr3 (Fgfr3Act) and from wildtype (WT) mice with normal expression of Fgfr3. Total RNA from these murine dermal fibroblasts (passage 4) were extracted and after quality control, were hybridized to the murine genome U74 gene chip. We have identified that Fgfr3 regulates important profibrotic pathways in fibroblasts. Selective upregulation of fibroblast growth factor receptor 3 (FGFR3) and its ligand FGF9 promote fibroblast activation and tissue fibrosis Transcriptome profiling, in silico analysis and functional experiments revealed that FGFR3 synergistically induces multiple profibrotic pathways including Endothelin-, Interleukin-4- and CTGF-signaling in a CREB-dependent manner. Inhibition of FGFR3 signaling by fibroblast-specific knockout of FGFR3 or FGF9 or pharmacological inhibition of FGFR3 inhibited fibroblast activation and attenuated experimental skin fibrosis. We have characterized FGFR3 as an upstream regulator of a network of profibrotic mediators and as a potential target for the treatment of fibrosis.

2020-10-01 | GSE148643 | GEO

Microarray of Human astrocytes transduced with lentivirus expressing FGFR3-TACC3 treated with vehicle, FGFR3-TACC3 treated with the FGFR inhibitor PD173074 for 12h, FGFR3-TACC3-K508M treated with vehicle or empty vector treated with vehicle

Project description:In order to interrogate the transcriptional changes elicited by FGFR3-TACC3, we expressed the FGFR3-TACC3 fusion protein in human astrocytes and compared the global gene expression profiles of cells treated with a specific inhibitor of FGFR3-TK (PD173074) or vehicle. FGFR3-TACC3 expressing HA were also compared with HA that expressed the kinase-inactive FGFR3-TACC3 (FGFR3-TACC3-K508M) and HA transduced with the empty vector. Gene Ontology-guided enrichment map demonstrated that, besides the expected enrichment for mitotic activity, oxidative phosphorylation and mitochondrial biogenesis were the most significant biological functions enriched in HA expressing active FGFR3-TACC3.

2017-10-17 | E-MTAB-6037 | biostudies-arrayexpress

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