The CPSF7 Knockout Raji Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout population derived from the Raji human B lymphocyte suspension cell line. These cells carry a disrupted CPSF7 gene via CRISPR/Cas9-mediated gene disruption, resulting in a heterogeneous pool with loss of CPSF7 function. This polyclonal format avoids clonal selection bias and offers a robust model for studying CPSF7 in pre-mRNA 3?? end processing and alternative polyadenylation.
The Raji cell line, a widely used Burkitt??s lymphoma model, is EBV-positive and lymphoblastoid, exhibiting suspension growth and constitutive oncogenic signaling, notably driven by MYC. It provides a disease-relevant background for investigating CPSF7, as dysregulation of alternative polyadenylation is common in B-cell malignancies and contributes to oncogenic mRNA isoform expression.
CPSF7 is an essential subunit of the Cleavage Factor Im (CFIm) complex that, together with NUDT21 (CFIm25), binds UGUA motifs upstream of polyadenylation sites, directing alternative polyadenylation and modulating 3??UTR length. This regulation impacts mRNA stability, localization, and translation efficiency. CPSF7 interacts with CSTF2, CPSF1, RNA polymerase II, and splicing factors, linking 3?? end processing to gene expression output. Upstream regulators MYC and NF-??B, along with cell cycle regulators, converge on this pathway, while downstream targets include CCND1, BCL2, and CD19, whose mRNA isoforms undergo CPSF7-dependent alternative polyadenylation. Thus, CPSF7 serves as a node integrating oncogenic signaling with mRNA isoform regulation.
In the Raji B lymphoma model, disruption of CPSF7 enables dissection of alternative polyadenylation??s contribution to lymphomagenesis. MYC overexpression and aberrant cell cycle progression in Burkitt??s lymphoma are influenced by 3??UTR-mediated gene regulation. The knockout model exposes how shifts in polyadenylation site usage affect oncogene and tumor suppressor expression, potentially revealing isoform-specific vulnerabilities. The polyclonal population mirrors tumor heterogeneity, supporting studies on proliferation and apoptosis pathways relevant to B-cell lymphoma biology.
Applications include genome-wide profiling of polyadenylation changes via RNA-seq and 3??READS, validation of target expression changes (e.g., CCND1 and BCL2) by Western blotting and RT-qPCR, and functional assays such as flow cytometry for proliferation and apoptosis. These enable research in functional genomics, alternative polyadenylation mechanisms, drug target validation, and gene expression regulation in B-cell malignancies. For additional technical details or ordering information, please contact Ascent Research.
