The PCDH1 Knockout Raji Polyclonal Cells are a CRISPR/Cas9-edited polyclonal cell population with targeted disruption of the human PCDH1 gene in the Raji B lymphocyte line. PCDH1 encodes protocadherin-1, a calcium-dependent cell-cell adhesion protein with proposed tumor-suppressive functions. This polyclonal knockout model provides a heterogeneous loss-of-function background suitable for investigating PCDH1 roles in adhesion, signaling, and disease without requiring single-cell clone isolation.
Raji is an EBV-positive Burkitt lymphoma-derived B cell line widely employed in immunological and cancer research. Originating from B lymphocytes, these cells are capable of antibody production and serve as a model for immune surveillance mechanisms. Their rapid proliferation and well-characterized genetics make them a robust host for gene-editing studies, while EBV positivity introduces distinct transcriptional features relevant to host-pathogen interactions.
PCDH1 functions as a calcium-dependent homophilic adhesion protein that forms complexes with ??-catenin, ??-catenin, and p120 catenin at cell?Ccell junctions. Through these interactions, PCDH1 inhibits ??-catenin-mediated transcriptional activation downstream of Wnt ligands and Frizzled receptors, thereby suppressing TCF/LEF target gene expression. Loss of PCDH1, often through promoter hypermethylation, disrupts cadherin-mediated adhesion, promotes ??-catenin signaling, and dysregulates downstream effectors such as actin cytoskeleton remodeling and cell cycle regulators p21 and p27. This network establishes PCDH1 as a tumor suppressor whose silencing favors epithelial-mesenchymal transition and oncogenic progression.
In the Raji B lymphocyte context, the PCDH1 knockout model enables dissection of adhesion-dependent processes in a hematopoietic background, despite the non-epithelial lineage. The loss-of-function phenotype may illuminate roles for protocadherin-1 in lymphoma cell?Ccell interactions, immune synapse formation, or microenvironment crosstalk. Given the documented loss of PCDH1 in breast, lung, colorectal, and gastric cancers, this model offers a surrogate system to probe aberrant cadherin signaling and tumor suppressor networks, potentially revealing therapeutic vulnerabilities.
Researchers can employ these polyclonal knockout cells in a range of assays: cell aggregation and transwell migration assays to quantify adhesion and EMT-like behavior; co-immunoprecipitation and immunofluorescence to analyze ??-catenin and actin cytoskeleton dynamics; ??-catenin/TCF/LEF reporter assays to measure transcriptional activity; and proliferation/apoptosis assays to assess cell cycle involvement. Epigenetic studies may use ChIP-qPCR and RT-qPCR to examine promoter methylation and mRNA expression. The model is also suitable for drug screening to identify PCDH1 re-expression agents. For more information or to place an order, please contact Ascent Research.
