FGFR3 Knockout 5637 Cell Line is a human CRISPR/Cas9-engineered bladder carcinoma cell model in which the FGFR3 gene has been disrupted to abolish functional FGFR3 expression. The edited line provides a stable in vitro system for investigating FGFR3-dependent signaling and phenotype in a urothelial epithelial-derived tumor background. This product is intended for mechanistic studies in cancer biology, receptor tyrosine kinase signaling, and therapeutic response, where controlled loss of FGFR3 enables direct assessment of pathway contribution in a disease-relevant cellular context.
The parental 5637 cell line is a human urinary bladder carcinoma epithelial cell line with established utility in studies of urothelial cancer biology. Because 5637 cells retain features relevant to bladder tumor growth, signaling regulation, and drug response, they are frequently used to examine oncogenic receptor signaling, proliferation control, and treatment-associated phenotypes. As an experimentally tractable urothelial tumor model, 5637 supports investigation of how receptor tyrosine kinases integrate extracellular cues with intracellular survival and differentiation programs.
FGFR3 encodes a fibroblast growth factor receptor tyrosine kinase activated by FGF ligands including FGF1, FGF2, FGF9, and FGF18 in the presence of heparan sulfate proteoglycan cofactors. Ligand binding promotes FGFR3 dimerization and autophosphorylation, creating docking sites for signaling mediators such as FRS2 and SHC1. These complexes recruit GRB2-SOS1 and PTPN11/SHP2 to stimulate the RAS-RAF1-MAP2K1/MEK1-MAPK1/ERK2 cascade, while parallel coupling to GAB1 and PIK3CA-AKT1 promotes PI3K-AKT-mTOR signaling. FGFR3 also interacts with PLCG1 and can engage STAT1 and STAT3 signaling outputs linked to proliferation, survival, and differentiation. Negative regulatory influences within this network include CBL, SPRY2, and SEF/IL17RD. Dysregulated FGFR3 signaling is highly relevant to bladder cancer and urothelial carcinoma, and is also broadly connected to skeletal dysplasia syndromes such as achondroplasia and thanatophoric dysplasia.
In the 5637 background, FGFR3 knockout is useful for defining how loss of this receptor reshapes urothelial carcinoma signaling architecture, including attenuation of ERK1/2, AKT, PLCgamma, and STAT pathway responses downstream of FGF stimulation. This host-target combination enables analysis of FGFR3-dependent cell-cycle progression, survival responses, and pathway cross-talk with other receptor tyrosine kinase inputs, while also supporting studies of adaptive signaling and therapeutic sensitivity.
Applications include western blot or phospho-signaling analysis of FGFR, ERK, and AKT pathway activity after ligand stimulation; RT-qPCR and RNA-seq profiling of transcriptional changes associated with receptor loss; and co-immunoprecipitation studies of signaling complexes involving FRS2, GRB2, SHC1, or PLCG1. The model is also suited to cell proliferation, colony formation, apoptosis, and cell-cycle assays to quantify functional dependency on FGFR3, as well as migration, invasion, reporter-based pathway analysis, flow cytometry, immunofluorescence, and drug sensitivity studies evaluating response or resistance to targeted inhibitors in bladder cancer research. Researchers may contact Ascent Research for additional technical information, product details, or related gene-edited cell models.
