This product is a CRISPR/Cas9-edited polyclonal knockout population of the CBX6 gene in HGC-27 human gastric carcinoma cells. The polyclonal format provides a heterogeneous loss-of-function model, obviating clonal selection artifacts. It is designed for functional studies of CBX6-dependent epigenetic regulation and its role in cancer biology.
The HGC-27 host cell line is a human undifferentiated gastric carcinoma epithelial line derived from a metastatic lymph node. It is widely used to model invasive gastric cancer, particularly for studying metastatic progression and cancer stem cell traits. This line??s aggressive phenotype makes it suitable for exploring epigenetic mechanisms of gastric oncogenesis and testing epigenetic therapies.
CBX6 (Chromobox 6) is a key component of the Polycomb repressive complex 1 (PRC1), where it functions as an H3K27me3 reader via its N-terminal chromodomain. Upon binding to trimethylated lysine 27 of histone H3, CBX6 facilitates the recruitment of core PRC1 subunits including RING1A/B E3 ubiquitin ligases, PHC1-3, and PCGF proteins such as BMI1. This assembly catalyzes the monoubiquitination of histone H2A at lysine 119 (H2AK119ub), a modification that promotes chromatin compaction and stable gene silencing. CBX6-mediated repression is regulated upstream by the E2F1 transcription factor and MAPK/ERK signaling, while downstream targets encompass CDKN2A (p16/INK4a), HOX gene clusters, and additional developmental and tumor suppressor genes. The CBX6-PRC1 axis thus integrates developmental cues and oncogenic signals to silence key regulatory loci.
In the context of HGC-27 gastric cancer cells, CBX6 is implicated in maintaining an undifferentiated, stem-like phenotype through epigenetic repression of tumor suppressors. Disruption of CBX6 via CRISPR/Cas9 in this model system is expected to relieve PRC1-dependent silencing of CDKN2A and other antiproliferative genes, potentially reducing cell growth, clonogenicity, and invasive capacity. This polyclonal knockout further enables investigation into the epigenomic landscape of gastric cancer and the dependency of cancer stem cell programs on CBX6-containing PRC1 complexes. The model thus provides a valuable tool for dissecting the interplay between chromatin regulation and oncogenesis in a metastatic gastric cancer background.
Researchers can employ this CBX6 knockout HGC-27 polyclonal cell population in a wide array of assays to probe epigenetic mechanisms in gastric cancer. Representative experimental approaches include western blotting to assess CBX6 and H2AK119ub levels, RT-qPCR for quantifying derepression of CDKN2A and HOX genes, and chromatin immunoprecipitation followed by qPCR (ChIP-qPCR) to map changes in H3K27me3 occupancy and CBX6 chromatin binding. Functional readouts such as MTT or colony formation assays, transwell migration and invasion assays, and flow cytometric analysis of cancer stem cell markers (e.g., CD44, ALDH) can be coupled with transcriptome-wide profiling via RNA-seq to comprehensively characterize the consequences of CBX6 loss. These applications support research in epigenetic drug screening and the identification of novel vulnerabilities in gastric cancer. For further details or to discuss custom applications, please contact Ascent Research.
