The CBX8 Knockout Jurkat Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population featuring targeted disruption of the CBX8 gene in the Jurkat T-cell leukemia line. This polyclonal pool enables loss-of-function studies for CBX8, a core Polycomb repressive complex 1 (PRC1) component. The heterogeneous population is suitable for assessing CBX8-dependent phenotypes without single-clone bias. The knockout model, generated via CRISPR/Cas9 gene disruption, provides a versatile tool for dissecting CBX8 functions in chromatin regulation and oncogenic signaling.
The Jurkat host cell line, derived from a 14-year-old male with acute T-cell leukemia, is a well-established T-lymphocyte model that recapitulates T-cell signaling, including TCR-mediated activation, IL-2 production, and apoptosis regulation. Its well-characterized genetic and epigenetic landscape makes it ideal for studying hematological malignancies, particularly T-cell acute lymphoblastic leukemia (T-ALL). Integrating CBX8 knockout into Jurkat cells allows precise investigation of Polycomb-mediated gene silencing within a T-cell context, relevant to both normal development and leukemogenesis.
CBX8 functions as a chromatin reader and transcriptional repressor, binding histone H3K27me3 via its chromodomain and directing PRC1-mediated monoubiquitination of H2A at lysine 119 (H2AK119ub). This compaction silences target loci, including the CDKN2A and CDKN2B tumor suppressors, thereby promoting cell cycle progression and inhibiting senescence. CBX8 operates downstream of MYC and Wnt/??-catenin signaling, and interacts with BMI1, RING1B, PHC1, and RYBP within PRC1. Dysregulation of CBX8 has been linked to poor prognosis in acute myeloid leukemia, breast, hepatocellular, and colorectal carcinomas.
In Jurkat T-ALL cells, CBX8 likely maintains leukemic phenotypes by repressing growth inhibitory and pro-apoptotic genes. Disruption of CBX8 is expected to relieve PRC1 silencing at CDKN2A and HOXA cluster loci, potentially restoring cell cycle checkpoints and enhancing apoptotic sensitivity. This knockout model enables detailed study of epigenetic dependencies in T-cell leukemia and serves as a platform for PRC1 inhibitor screening. Additionally, the role of CBX8 in MYC-driven oncogenesis can be explored, revealing combinatorial therapeutic vulnerabilities.
The CBX8 Knockout Jurkat Polyclonal Cells support diverse assays including ChIP-qPCR for H3K27me3 and CBX8 occupancy, RT-qPCR for target gene derepression, and Western blotting for PRC1 component analysis. Functional assays such as proliferation, apoptosis, and flow cytometric cell cycle analysis quantify biological effects. Transcriptome-wide RNA sequencing can identify broader regulatory changes, facilitating research into drug resistance and epigenetic signaling. For further details, please contact Ascent Research.
