The FNDC3A Knockout Raji Polyclonal Cells are a CRISPR/Cas9-edited polyclonal population generated from the Raji B-lymphoblast cell line, enabling targeted disruption of the FNDC3A gene. This polyclonal format provides a heterogeneous knockout model without clonal selection, reflecting a spectrum of editing outcomes suitable for population-level functional assays in lymphoid cancer research.
Raji cells originate from an EBV-positive Burkitt’s lymphoma and serve as a classic model for B-cell malignancies. They display mature B-cell characteristics and exhibit integrin-dependent adhesion and signaling networks. Their extensive use in cancer biology and immunology provides a robust background for interrogating gene function in lymphoma and leukemia contexts.
FNDC3A encodes a fibronectin type III domain protein that orchestrates cell-extracellular matrix interactions through integrin signaling. It physically interacts with integrin subunits ITGB1 and ITGAV and with talin and fibronectin, promoting downstream activation of FAK and SRC. These kinases regulate Rho GTPases including RhoA, RAC1, and CDC42, thereby controlling focal adhesion dynamics, actin cytoskeleton reorganization, and cell motility. This molecular framework positions FNDC3A as a critical node in adhesion-dependent signaling, with implications for both normal and malignant B-cell physiology. Consequently, FNDC3A integrates adhesive and growth factor signals to modulate proliferation and migration.
In Raji cells, FNDC3A disruption is anticipated to impair integrin-mediated adhesion and signaling, directly impacting pathways that sustain anchorage-independent growth and tissue infiltration. Given the role of FAK/SRC signaling in lymphoma cell survival and dissemination, this knockout model allows dissection of FNDC3A-dependent contributions to malignant phenotypes without clonal bias. By providing a loss-of-function system in a well-characterized B-lymphoma background, the model supports mechanistic studies of how FNDC3A coordinates extracellular signals to influence cytoskeletal remodeling and gene expression programs in Burkitt lymphoma.
These polyclonal knockout cells are suitable for adhesion assays on ECM components, transwell migration and invasion studies, and proliferation analyses via MTT or XTT. Western blotting for phospho-FAK and phospho-SRC, along with flow cytometry of integrin expression, can quantify signaling changes. Application in drug sensitivity screens and tumor microenvironment interaction studies may uncover FNDC3A-dependent vulnerabilities. For additional information or inquiries, please contact Ascent Research.
