Homo sapiens
Ontology highlight
ABSTRACT:
OTHER RELATED OMICS DATASETS IN: GSE84733
PROVIDER: PRJNA330970 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Gene expression data from RT112 following FGFR3 knock-down using FGFR3 siRNAs
| PRJNA330969 | ENA
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:Gene expression data from UMUC-14 following FGFR3 knock-down using FGFR3 siRNAs
| PRJNA516796 | ENA
Project description:Gene expression data from MGH-U3, RT112 and UM-UC-5 following TYRO3 knock-down
| PRJNA390518 | ENA
Project description:To better understand the molecular mechanisms underlying TYRO3 oncogenic activity in bladder carcinomas, we made use of MGH-U3, RT112 and UM-UC-5 cell lines, which were derived from a human bladder tumor and endogenously expressed the Tyro3 protein, the growth and transformation of these cell lines being dependent on Tyro3. We carried out a gene expression analysis using Affymetrix DNA arrays in this cell line treated or not withTYRO3 siRNAs.
2019-02-27 | GSE100025 | GEO
Project description:FGFR3 (Fibroblast Growth Factor Receptor 3) is one of the most frequently altered genes in bladder cancer, primarily through activating mutations that drive oncogenesis and are enriched in luminal tumors. However, the underlying gene regulatory network (GRN) remains poorly characterized. Here, we inferred an FGFR3-mutated GRN using a bottom-up bioinformatics approach, integrating transcriptomic data from bladder cancer cell lines, FGFR3-mutated tumors, and FGFR3-perturbation experiments in human and mouse models. Using CRISPR-Cas9 screen public data, we identified transcription factors (TFs) from this GRN that regulate the viability of FGFR3-mutated cells, with a focus on p63 (TP63). We showed that FGFR3 activation upregulates p63 in patient-derived xenografts and cell lines, while single-cell RNA sequencing revealed heterogeneous p63 activation associated with basal differentiation. Functional studies, including TP63 knock-down in FGFR3-dependent in vitro and in vivo models and RNA-seq along with p63 ChIP-seq, demonstrated that p63 directly promotes cell proliferation and migration, and uncovered a positive feedback loop between FGFR3 and p63. Together, these findings identified p63 as a pro-tumorigenic regulator in FGFR3 mutated tumors despite their luminal differentiation and provide a detailed FGFR3-driven GRN, offering insights into FGFR3-induced oncogenic dependency and potential strategies to circumvent resistance to FGFR inhibitors.
2026-01-06 | GSE315628 | GEO
Project description:FGFR3 (Fibroblast Growth Factor Receptor 3) is one of the most frequently altered genes in bladder cancer, primarily through activating mutations that drive oncogenesis and are enriched in luminal tumors. However, the underlying gene regulatory network (GRN) remains poorly characterized. Here, we inferred an FGFR3-mutated GRN using a bottom-up bioinformatics approach, integrating transcriptomic data from bladder cancer cell lines, FGFR3-mutated tumors, and FGFR3-perturbation experiments in human and mouse models. Using CRISPR-Cas9 screen public data, we identified transcription factors (TFs) from this GRN that regulate the viability of FGFR3-mutated cells, with a focus on p63 (TP63). We showed that FGFR3 activation upregulates p63 in patient-derived xenografts and cell lines, while single-cell RNA sequencing revealed heterogeneous p63 activation associated with basal differentiation. Functional studies, including TP63 knock-down in FGFR3-dependent in vitro and in vivo models and RNA-seq along with p63 ChIP-seq, demonstrated that p63 directly promotes cell proliferation and migration, and uncovered a positive feedback loop between FGFR3 and p63. Together, these findings identified p63 as a pro-tumorigenic regulator in FGFR3 mutated tumors despite their luminal differentiation and provide a detailed FGFR3-driven GRN, offering insights into FGFR3-induced oncogenic dependency and potential strategies to circumvent resistance to FGFR inhibitors.
2025-12-28 | GSE314908 | GEO
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.
2020-12-31 | GSE125547 | GEO