The PBX3 Knockout Raji Polyclonal Cells provide a CRISPR/Cas9-mediated loss-of-function model of the PBX3 gene in the human Raji B lymphocyte line. This polyclonal knockout population is generated through targeted disruption of the PBX3 locus, yielding a heterogeneous pool of edited cells that collectively mirror PBX3 deficiency. Unlike single-cell clones, the polyclonal format preserves population variability, suitable for studying pooled knockout effects in a lymphoma context, and enables interrogation of PBX3-dependent transcriptional networks without monoclonal bias.
The Raji host cell line is an EBV-positive B lymphocyte line derived from a Burkitt lymphoma patient. Raji cells are widely used in immunological and oncological research for their roles in immune surveillance, antibody production, and antigen presentation. Their lymphoblastoid phenotype and latent EBV infection confer distinct signaling properties relevant for investigating B cell malignancies, offering a tractable model of aggressive lymphoma to examine transformed B cell behavior and host-viral interactions in tumorigenesis.
PBX3 encodes a transcription factor that functions as a cofactor for HOX proteins and participates in the HOX-PBX-MEIS transcriptional network. It forms heterodimeric or heterotrimeric complexes with HOX family members such as HOXA9 and HOXB4, and with MEIS1 and PREP1 cofactors, to regulate downstream gene expression. Upstream signals including FGF and BMP converge on PBX3 via the Wnt/??-catenin and TGF-??/SMAD pathways, where ??-catenin and SMAD2/3 modulate its activity. Activated PBX3 complexes bind target loci and drive transcription of oncogenes c-MYC and CCND1, while also influencing BCL2 and CDKN1A, thereby promoting cell cycle progression and suppressing apoptosis.
In the Raji B cell context, PBX3 is implicated in maintaining oncogenic programs relevant to Burkitt lymphoma and other B cell malignancies. CRISPR/Cas9 disruption of PBX3 dismantles key transcriptional complexes, impairing expression of proliferative and anti-apoptotic targets. Consequently, PBX3 knockout Raji polyclonal cells may exhibit reduced proliferation, altered cell cycle profiles, and heightened apoptosis susceptibility. This model is valuable for dissecting transcriptional dependencies in aggressive lymphomas and exploring PBX3’s role in acute lymphoblastic leukemia, colorectal cancer, and gastric cancer.
Researchers can use PBX3 Knockout Raji Polyclonal Cells in diverse functional assays for transcription factor biology, oncogene regulation, and drug target validation. Representative techniques include RT-qPCR and Western blotting to confirm PBX3 disruption and assess target expression; RNA-seq for transcriptomic profiling; ChIP-qPCR for target occupancy; and flow cytometry for apoptosis and cell cycle analysis. Proliferation and reporter assays further support kinetic and mechanistic studies. This polyclonal knockout population is a versatile tool for advancing lymphoma research and targeted therapy development. For details, contact Ascent Research.
