The CBX6 Knockout Huh-7 Polyclonal Cells are a CRISPR/Cas9-edited human knockout cell population derived from the Huh-7 hepatocellular carcinoma line, with targeted disruption of the endogenous CBX6 gene. This polyclonal model provides a heterogeneous collection of CBX6-deficient cells, offering a powerful tool for investigating the role of CBX6 in chromatin biology and liver cancer without the limitations of clonal variability. It is ideal for pooled functional assays, epigenomic profiling, and drug sensitivity screens.
Huh-7 is a well-differentiated human hepatocellular carcinoma cell line established from a liver tumor in a 57-year-old Japanese male. It retains key hepatocytic features, including metabolic activity, protein synthesis capability, and susceptibility to hepatitis C virus (HCV) infection, making it a widely used model for liver cancer research and HCV?Chost interaction studies. The cells harbor wild-type TP53 and are genetically stable, providing a consistent background for gene-editing experiments aimed at dissecting oncogenic pathways and epigenetic dysregulation in hepatocellular carcinoma.
CBX6 encodes Chromobox Protein Homolog 6, a core component of the Polycomb Repressive Complex 1 (PRC1), which functions as a reader of the trimethylated histone H3 lysine 27 (H3K27me3) mark deposited by PRC2. CBX6 specifically recognizes H3K27me3 through its chromodomain and facilitates the recruitment of PRC1 catalytic subunits RING1B and BMI1 to chromatin, promoting monoubiquitination of histone H2A at lysine 119 (H2AK119ub). This post-translational modification locks target genes in a transcriptionally repressed state, silencing key tumor suppressors such as CDKN2A/p16INK4a and CDKN1A/p21. Upstream, CBX6 expression and PRC1 activity are modulated by PRC2 component EZH2 and by signaling cascades including AKT and MAPK pathways. CBX6 functions within a network that includes interactions with RING1A/RING1B, PHC1-3, MEL18/PCGF2, and RYBP, collectively mediating epigenetic maintenance of stem cell pluripotency and cell cycle regulation.
In hepatocellular carcinoma, aberrant expression of Polycomb group proteins drives tumor progression by enforcing silencing of antiproliferative and pro-apoptotic genes. CBX6 is implicated in liver cancer through its role in PRC1-mediated chromatin compaction, which may promote oncogenic phenotypes by sustaining repression of tumor suppressor loci. The Huh-7 polyclonal CBX6 knockout model enables dissection of CBX6-specific contributions to epigenetic regulation and hepatocellular carcinogenesis, distinct from other PRC1 components, and allows assessment of its therapeutic vulnerability in a clinically relevant liver cancer cell background.
This knockout product is suited for a wide range of applications in liver cancer biology and epigenetics, including chromatin immunoprecipitation (ChIP) to map CBX6 occupancy and H3K27me3/H2AK119ub distributions, RT-qPCR and RNA-seq for gene expression profiling of Polycomb targets, and proliferation, colony formation, or xenograft assays to evaluate tumorigenicity. Additional uses include immunofluorescence and co-immunoprecipitation to study protein interactions within the PRC1 complex. For further inquiries, contact Ascent Research.
