LAMC1 Knockout Raji Polyclonal Cells constitute a CRISPR/Cas9-edited polyclonal knockout population generated from the human Raji B lymphocyte line, designed to disrupt the LAMC1 gene encoding the laminin subunit gamma-1. This heterogeneous pool preserves cellular diversity while providing a loss-of-function model for investigating LAMC1-dependent biological processes, circumventing clonal selection biases and enabling robust functional studies in a lymphoid background.
The Raji cell line is a well-characterized suspension B lymphocyte model derived from a Burkitt lymphoma patient, extensively utilized in immunology and cancer research. These cells retain hallmarks of B cell biology, including surface immunoglobulin expression and integrin-mediated adhesion properties, making them particularly relevant for dissecting how extracellular matrix interactions influence lymphoma cell behavior, survival, and migration.
LAMC1 encodes the gamma-1 chain of laminin, a central basement membrane glycoprotein that assembles with alpha and beta subunits into heterotrimers such as laminin-111. Through binding to integrin receptors??including ??6??1 and ??3??1??and coreceptors like dystroglycan and nidogen, laminin activates intracellular signaling cascades. Downstream, it promotes phosphorylation of focal adhesion kinase (FAK), Src, ERK1/2, and Akt, while also engaging Rac1 to regulate cytoskeletal remodeling. Transcriptional control of LAMC1 is driven by upstream regulators TGF-??, EGF, SP1, and AP-1.
In the Raji context, disruption of LAMC1 is predicted to attenuate integrin-dependent adhesion and downstream signaling, potentially impairing FAK, Src, ERK, and Akt pathway activation. Since B lymphocyte trafficking and lymph node retention rely on laminin-integrin interactions, this knockout model offers a pertinent system to examine how the laminin gamma-1 subunit contributes to lymphoma cell anchorage, migration, and survival within the tumor microenvironment.
Researchers can apply these cells in diverse experimental workflows: Western blotting and RT-qPCR for confirming LAMC1 disruption, flow cytometry to monitor integrin surface expression, adhesion and transwell migration/invasion assays to evaluate functional outcomes, and phospho-signaling analyses to map pathway alterations. The model is suited for exploring cancer cell-ECM crosstalk, drug sensitivity screening, fibrosis mechanisms, and metastasis biology. For additional information or technical support, please contact Ascent Research.
