The PCDHB3 Knockout Raji Polyclonal Cells product comprises a CRISPR/Cas9-edited polyclonal knockout cell population derived from the Raji B lymphoblast cell line, engineered for loss-of-function studies of the human PCDHB3 gene. This polyclonal pool contains a heterogeneous mixture of cells carrying various disruptions in the PCDHB3 locus, enabling robust assessment of gene function without clonal bias. The knockout model provides a versatile tool for investigating the role of PCDHB3 in cell adhesion and signaling pathways relevant to B-cell malignancies.
The Raji host cell line is an Epstein-Barr virus (EBV)-positive Burkitt lymphoma-derived B lymphoblast line that serves as a widely used model for B-cell lymphoma and immune signaling studies. Raji cells express surface markers characteristic of mature B lymphocytes and maintain key signaling networks, including NF-??B and Wnt pathways, that are frequently dysregulated in lymphomagenesis. The EBV-immortalized nature of Raji cells offers a physiologically relevant context to examine oncogenic mechanisms and therapeutic vulnerabilities.
PCDHB3 encodes a protocadherin family member that mediates calcium-dependent homophilic cell-cell adhesion and has been implicated as a tumor suppressor in multiple cancers, including B-cell malignancies. Its expression is often silenced by DNMT1/DNMT3B-mediated promoter methylation. In the Wnt/??-catenin pathway, PCDHB3 interacts with ??-catenin and ??-catenin, promoting sequestering at the membrane and thereby limiting nuclear ??-catenin accumulation. Loss of PCDHB3 disrupts cadherin-mediated adhesion, stabilizes ??-catenin, and enhances transcription of Wnt target genes such as cyclin D1 and c-MYC. Additionally, PCDHB3 functions regulate gamma-secretase?Cmediated processing and downstream caspase activation.
In the Raji cellular context, knockout of PCDHB3 abrogates homophilic cell adhesion and relieves inhibition of Wnt/??-catenin signaling, leading to enhanced ??-catenin stabilization and transcriptional activation of pro-proliferative and anti-apoptotic genes. This mimics epigenetic silencing events observed in Burkitt lymphoma and other B-cell tumors, making the model highly relevant for dissecting tumor suppressor mechanisms. The polyclonal population captures diverse allelic disruptions, enabling functional genomics and drug response studies in a heterogeneous tumor-like background.
This knockout cell product is suitable for investigating PCDHB3 tumor suppressor function through assays such as Western blotting for ??-catenin and cyclin D1, RT-qPCR for Wnt target genes, cell proliferation (MTS/ATP), apoptosis (Annexin V), and adhesion assays. It facilitates screening of epigenetic reactivation agents like 5-aza-2′-deoxycytidine, methylation-specific PCR, RNA-seq profiling, and flow cytometric cell cycle analysis. Moreover, the model supports drug sensitivity and resistance studies in B-cell lymphoma. For further technical details and ordering information, please contact Ascent Research.
