The NID2 Knockout Raji Polyclonal Cells consist of a CRISPR/Cas9-edited polyclonal population derived from the Raji B lymphoblast line. This model employs CRISPR/Cas9-mediated gene disruption to ablate NID2 function, generating a heterogeneous knockout pool that avoids clonal selection bias. The polyclonal format facilitates robust loss-of-function studies while capturing cellular variability. These cells are provided as a ready-to-use tool for investigating extracellular matrix interactions and lymphoma biology.
Raji is a human B lymphoblast cell line originating from a Burkitt lymphoma patient, characterized by EBV positivity and retention of B cell features such as surface immunoglobulin expression. This cell line is a well-established model for studying lymphomagenesis, immune signaling, and tumor microenvironment dynamics. Its aggressive lymphoma background makes it particularly suitable for dissecting pathways involved in cancer cell adhesion, migration, and stromal interactions.
The NID2 gene product, nidogen-2, is a basement membrane glycoprotein that non-covalently bridges laminin and type IV collagen networks, thereby stabilizing cell-matrix interactions. Nidogen-2 is regulated by TGF-beta signaling and mechanical cues like ECM stiffness, and it converges on integrin activation and focal adhesion kinase (FAK) phosphorylation. It interacts directly with laminin isoforms, collagen IV, perlecan, and fibronectin, and modulates integrin-mediated cascades involving Src and paxillin. Consequently, NID2 loss impairs adhesion-dependent signaling, cell spreading, and migration by disrupting the structural and signaling roles of the basement membrane.
In Raji B lymphoma cells, NID2 knockout disrupts the pericellular matrix, compromising integrin-mediated adhesion and focal adhesion dynamics. This disruption likely alters adhesion-dependent survival pathways and migratory behavior, influencing the capacity for lymphoma cell dissemination and microenvironmental crosstalk. The model enables interrogation of how basement membrane components contribute to lymphomagenic processes and the tumor niche, providing insights into ECM remodeling and therapeutic vulnerabilities.
Researchers can employ this knockout model in lymphoma biology, cell-ECM adhesion studies, and tumor microenvironment investigations. Representative assays include Western blotting for ECM proteins, adhesion assays on laminin/collagen substrates, Transwell migration/invasion assays, immunofluorescence for focal adhesion markers (paxillin, vinculin), flow cytometry for integrin levels, and transcriptomic analyses. For further details, contact Ascent Research.
