The FILIP1L Knockout Raji Polyclonal Cells comprise a CRISPR/Cas9-edited polyclonal knockout cell population derived from the Raji B lymphocyte cell line. This product provides a genetically disrupted model of the FILIP1L gene, enabling loss-of-function studies. The polyclonal format captures a diverse array of editing events across the cell population, facilitating robust functional characterization without single-cell cloning. These cells are suitable for investigating tumor-suppressive mechanisms mediated by FILIP1L in a B cell lymphoma background.
Raji cells are a widely utilized human B lymphocyte line originally established from a Burkitt??s lymphoma patient. As a model for B cell malignancies, Raji cells recapitulate key features of aggressive lymphomas and serve as a platform for immunological and oncogenic signaling research. Their rapid proliferation and defined genetic background make them ideal for CRISPR-based gene disruption studies aimed at dissecting molecular pathways in B cell lymphomagenesis.
FILIP1L (Filamin A Interacting Protein 1-Like) functions as a putative tumor suppressor, exerting its effects primarily through interaction with Filamin A (FLNA) and modulation of the actin cytoskeleton. By binding FLNA, FILIP1L regulates actin dynamics, thereby inhibiting cell migration and invasion. Its expression is frequently silenced in cancers via promoter methylation, and its re-expression triggers apoptosis through caspase-3/7 activation. Upstream, TGF-?? signaling via SMAD2/3 can transcriptionally modulate FILIP1L, while downstream effects impinge on ??-catenin signaling and actin reorganization. The mechanistic network positions FILIP1L at the intersection of TGF-??-mediated growth suppression and cytoskeletal control.
In the Raji lymphoma context, disruption of FILIP1L allows researchers to explore how loss of this tumor suppressor contributes to B cell lymphoma progression. The knockout model is particularly relevant for studying evasion of apoptosis, enhanced migratory capacity, and altered signaling through TGF-?? pathways??features that are often dysregulated in Burkitt??s lymphoma and other B cell malignancies. Combined with Raji??s aggressive phenotype, this system provides a powerful tool to examine the functional consequences of FILIP1L silencing in a cancer cell environment where it is normally epigenetically downregulated.
Researchers can employ this polyclonal knockout population in a wide array of assays. For instance, Western blotting and RT-qPCR can confirm FILIP1L disruption, while RNA-seq reveals transcriptome-wide changes. Functional studies benefit from flow cytometric analysis of apoptosis (Annexin V/PI) and cell cycle, Transwell migration and invasion assays, and immunofluorescence to visualize actin cytoskeleton remodeling. Co-immunoprecipitation can verify loss of FILIP1L?CFLNA interaction. Moreover, these cells are suited for drug sensitivity screening to identify compounds that selectively target FILIP1L-deficient lymphomas. For further information, please contact Ascent Research.
