The EMP3 Knockout Raji Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population with targeted disruption of the EMP3 gene in the Raji human B lymphocyte line. This gene-edited cell pool provides a loss-of-function model to investigate EMP3-dependent processes without the need for single-cell cloning, enabling functional studies in a bulk population context.
The Raji cell line is derived from an Epstein-Barr virus (EBV)-positive Burkitt lymphoma and carries the characteristic t(8;14) c-MYC translocation. As a B lymphocyte model, Raji cells are widely used for studying antigen presentation, antibody production, and immune surveillance, offering a relevant background for exploring tumor-suppressive and adhesion mechanisms in lymphomagenesis.
EMP3 is a tetraspanin-associated membrane glycoprotein that modulates cell proliferation, adhesion, and apoptosis through integrin-mediated signaling. It interacts with integrin ??1 and tetraspanins such as CD9 and CD81, influencing downstream focal adhesion kinase (FAK) and Src family kinases, which in turn activate the PI3K/AKT and RAS/RAF/MEK/ERK cascades. EMP3 expression is frequently silenced by promoter methylation in cancer, and its re-expression can suppress tumor growth, implicating EMP3 as a context-dependent tumor suppressor that intersects with key proliferative and survival pathways.
In the Raji Burkitt lymphoma context, loss of EMP3 may alter integrin-mediated adhesion and downstream signaling, potentially affecting c-MYC-driven proliferation and immune interactions. Since EMP3 is epigenetically silenced in multiple cancers, this polyclonal knockout model allows dissection of EMP3’s role in B-cell lymphoma biology, including its impact on cell adhesion, migration, and apoptotic sensitivity, while maintaining the polyclonal heterogeneity of the original line.
Researchers can employ these EMP3 knockout Raji cells in a variety of functional assays, including Western blotting and phospho-immunoblotting to assess AKT and ERK1/2 activation, flow cytometry for surface integrin ??1 expression, and cell adhesion, migration, and apoptosis assays to evaluate tumor-suppressive mechanisms. The model is also suitable for RNA-sequencing-based transcriptomic profiling and for testing epigenetic therapies that reverse methylation silencing. For further information, please contact Ascent Research.
