The FGFR2 Knockout Raji Polyclonal Cells are a CRISPR/Cas9-mediated gene-disrupted polyclonal population derived from Raji B lymphocytes. This loss-of-function model for FGFR2 enables interrogation of receptor-dependent signaling and functions in a B-cell context. The polyclonal nature maintains genetic heterogeneity while abrogating target expression, suitable for comparative studies with wild-type Raji controls to dissect contributions to proliferation, survival, and signal transduction.
The parental Raji cell line is an Epstein-Barr virus (EBV)-positive lymphoblastoid line established from a Burkitt’s lymphoma patient. These B lymphocytes retain functional properties of antibody production, antigen presentation, and immune surveillance, making them a relevant model for studying B-cell physiology and lymphomagenesis. Raji cells express key B-cell markers and exhibit robust growth in suspension culture, facilitating high-throughput genetic and pharmacological screening. Their transformed phenotype also renders them sensitive to oncogene addiction, a feature advantageous for validating targeted therapies.
FGFR2 is a receptor tyrosine kinase that binds FGF ligands such as FGF1, FGF2, FGF7, and FGF10, with heparan sulfate proteoglycans as cofactors. Ligand-induced dimerization and autophosphorylation create docking sites for the adaptor protein FRS2, which recruits GRB2 and SOS to activate the RAS-MAPK pathway, leading to ERK1/2 phosphorylation and downstream expression of cyclin D1 and c-FOS. FRS2 further engages GAB1-PI3K, activating AKT and mTOR signaling to promote survival. Additionally, FGFR2 couples to PLC??1, triggering PKC activation and calcium release. Downstream effectors such as STAT3 and CRKL integrate with JAK/STAT and other pathways, placing FGFR2 at a central hub controlling proliferation, differentiation, and migration.
In the Raji B-lymphocyte background, FGFR2 disruption offers a unique window into FGF signaling within the immune compartment. While FGFR2 is broadly studied in epithelial cancers and skeletal disorders, its role in B-cell malignancies remains underexplored. Aberrant FGF signaling has been implicated in lymphomagenesis, and FGFR2 expression in lymphoid cells may contribute to tumor-stroma interactions or autonomous growth signals. By eliminating FGFR2 function in this polyclonal Raji model, researchers can assess its impact on B-cell viability, clonal expansion, and response to microenvironmental cues. This model also provides a platform to evaluate FGFR-targeted inhibitors, such as small-molecule kinase inhibitors or blocking antibodies, in a hematological cellular context.
The FGFR2 Knockout Raji Polyclonal Cells support diverse experimental workflows. Researchers can perform mechanistic studies using Western blotting, RT-qPCR, and RNA-seq to assess transcriptional and proteomic changes. Functional assays including proliferation, apoptosis, and drug sensitivity testing, coupled with phospho-ERK/AKT analysis by flow cytometry, enable quantitative signaling dissection. This model aids functional genomics screens and validation of FGFR2 as a therapeutic target in B-cell lymphomas, as well as co-culture studies of immune interactions. For more information or to discuss custom services, contact Ascent Research.
