The EDIL3 Knockout Raji Polyclonal Cells represent a CRISPR/Cas9-mediated polyclonal knockout population derived from the human Raji B lymphocyte cell line, in which the EDIL3 gene has been disrupted to create a loss-of-function model. This population, consisting of a heterogeneous mixture of edited alleles, provides a robust tool for studying EDIL3 function without clonal selection. The polyclonal format preserves genetic diversity and minimizes clonal artifacts, enabling broad functional assessment of EDIL3 deficiency in a lymphoma-relevant context.
The Raji cell line is a well-characterized EBV-positive Burkitt??s lymphoma model derived from a male patient, growing in suspension culture. These B lymphocytes express surface markers including IgM, CD19, and CD20, reflecting their mature B-cell origin. Raji cells are extensively used to investigate B-cell malignancies, EBV-driven lymphomagenesis, and immune cell signaling. Their EBV positivity and rapid proliferation make them an ideal host for studying oncogenic pathways and tumor biology, particularly in the context of lymphoma.
EDIL3 encodes a secreted extracellular matrix protein that functions as a ligand for integrins ??v??3, ??v??5, and ??4??1, mediating cell adhesion, angiogenesis, and immune modulation. EDIL3 is transcriptionally upregulated by proinflammatory and hypoxic stimuli such as TNF-??, IL-1??, TGF-??, and HIF-1?? via NF-??B and SP1. Upon integrin engagement, EDIL3 activates downstream signaling cascades including FAK/Src and PI3K/AKT/ERK pathways, leading to increased expression of matrix metalloproteinases MMP-2 and MMP-9 and the pro-angiogenic factor VEGF. By binding phosphatidylserine and integrins, EDIL3 also inhibits leukocyte-endothelial adhesion and promotes macrophage phagocytosis, thereby modulating immune responses within the tumor microenvironment.
In the Raji B-lymphoma context, EDIL3 elimination may impair integrin-mediated adhesion and signaling, potentially reducing tumor cell interactions with the microenvironment. Since EDIL3 promotes angiogenesis and immune evasion, its knockout could attenuate the supportive niche and alter sensitivity to microenvironment-derived signals. This model enables dissection of EDIL3-dependent oncogenic mechanisms, including integrin-driven survival and migration, and may reveal vulnerabilities in B-cell lymphoma. By combining this knockout with the EBV-positive background, researchers can explore the intersection of viral oncogenesis and EDIL3-mediated signaling.
Key applications include functional studies of EDIL3 in B-cell lymphoma pathogenesis, co-culture angiogenesis assays with endothelial cells, and adhesion assays to quantify integrin-dependent binding. The polyclonal population is suitable for drug sensitivity screening, cytokine profiling, apoptosis assays, and global gene expression analysis by RNA-seq, as well as protein-level validation by Western blotting and flow cytometry. These cells facilitate investigation of EDIL3??s role in tumor-stroma crosstalk and may aid in identifying therapeutic targets within integrin signaling pathways. For additional details, please contact Ascent Research.
