CBX6 Knockout Raji Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population derived from the human Raji B-lymphoblastoid cell line, featuring targeted disruption of the CBX6 gene. This loss-of-function model enables systematic investigation of CBX6-dependent molecular mechanisms without prior isolation of single-cell clones, providing a pooled population that reflects the heterogeneity essential for robust functional studies in cancer epigenetics.
The Raji host cell line is an EBV-positive Burkitt lymphoma-derived B-lymphoblastoid model widely used to study B-cell malignancies and Epstein-Barr virus latency programs. Characterized by a highly proliferative phenotype and constitutive MYC oncogene overexpression, Raji cells faithfully recapitulate key features of aggressive lymphomas and serve as a standard platform for pharmacological screening and mechanistic dissection of oncogenic signaling networks.
CBX6 (chromobox 6) is a core component of Polycomb repressive complex 1 (PRC1) that specifically recognizes trimethylated lysine 27 on histone H3 (H3K27me3), a repressive mark deposited by the PRC2 catalytic subunit EZH2. Upon binding to H3K27me3, CBX6 facilitates PRC1-mediated monoubiquitination of histone H2A at lysine 119 (H2AK119ub) via the E3 ligase activity of RING1B, leading to chromatin compaction and transcriptional silencing. CBX6 physically interacts with other PRC1 subunits such as BMI1/PCGF proteins and PHC family members, forming stable complexes that repress critical target loci including the CDKN2A tumor suppressor locus (encoding p16INK4a and p14ARF) and HOX developmental gene clusters. This molecular circuitry positions CBX6 at the nexus of H3K27me3 readout and downstream H2AK119ub-mediated gene repression, with functional consequences for cell cycle regulation, differentiation, and oncogenic transformation.
In the Raji B-cell lymphoma context, where aberrant Polycomb activity and H3K27me3 hypermethylation often coexist with MYC-driven transcriptional programs, CBX6 knockout disrupts PRC1-dependent silencing of tumor suppressors and differentiation genes, potentially impairing malignant cell growth and altering sensitivity to EZH2-targeted therapies. This polyclonal knockout population captures the biological variability of unselected gene disruptions, providing a physiologically relevant model to assess how CBX6 loss phenotypically impacts lymphoma viability, clonogenicity, and apoptotic signaling in an EBV-positive, MYC-overexpressing background. Such a model is instrumental for dissecting the interplay between PRC1 and PRC2 in B-cell lymphomagenesis and for evaluating the efficacy of epigenetic inhibitors.
These cells are suitable for a broad spectrum of experimental applications, including Western blotting to monitor H2AK119ub and H3K27me3 levels, RNA-sequencing to identify derepressed Polycomb target genes, chromatin immunoprecipitation sequencing (ChIP-seq) to map H3K27me3 and PRC1 genome-wide occupancy changes, and functional assays such as cell viability, apoptosis, flow cytometry, and drug sensitivity testing with EZH2 inhibitors. By enabling direct comparison between wild-type Raji and CBX6-disrupted populations, researchers can rigorously interrogate the epigenetic dependencies of B-cell lymphoma and accelerate the discovery of novel therapeutic vulnerabilities. For further details and ordering information, please contact Ascent Research.
