The CBX8 Knockout HGC-27 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal cell population derived from the HGC-27 human gastric carcinoma cell line, engineered for loss-of-function studies of CBX8. This product provides a heterogeneous pool of edited cells with targeted disruption of the CBX8 gene, enabling the investigation of CBX8-dependent functions without clonal selection.
The HGC-27 cell line originates from a metastatic lymph node of a patient with gastric adenocarcinoma and displays an undifferentiated, epithelial morphology. As a widely used model for gastric cancer, HGC-27 cells exhibit features of aggressive tumor behavior and serve as a relevant system for studying gastric carcinogenesis, metastasis, and drug response.
CBX8 functions as a core component of the Polycomb repressive complex 1 (PRC1), recognizing trimethylated histone H3 at lysine 27 (H3K27me3) via its chromodomain and facilitating the ubiquitination of histone H2A at lysine 119 (H2AK119ub). This activity maintains transcriptional silencing of target genes including CDKN2A (p16/INK4a), CDH1 (E-cadherin), and BAX. CBX8 interacts with PRC1 subunits BMI1, RING1B, and PHC, and is regulated by upstream factors such as E2F1, MYC, and the PI3K/AKT pathway, as well as by the PRC2 complex (EZH2/SUZ12/EED) that establishes H3K27me3. In gastric cancer, CBX8 overexpression promotes cell proliferation and epithelial?Cmesenchymal transition (EMT) through derepression of oncogenic effectors, linking CBX8 to pathways such as Wnt/??-catenin, where it modulates ??-catenin activity, and the PI3K/AKT signaling cascade, ultimately upregulating targets like CCND1 (cyclin D1) and SNAI1 (Snail).
In the context of HGC-27 gastric carcinoma cells, disruption of CBX8 provides a powerful tool to dissect the epigenetic mechanisms driving tumorigenesis. Loss of CBX8 is expected to de-repress tumor suppressor genes such as CDKN2A and CDH1, while attenuating oncogenic signaling through the Wnt/??-catenin and PI3K/AKT pathways. This model enables investigation of CBX8-mediated regulation of cell cycle, apoptosis, migration, and invasion, and can be used to evaluate the role of PRC1-dependent gene silencing in gastric cancer progression.
These CBX8 knockout polyclonal cells are suitable for a broad range of functional assays, including western blot analysis of CBX8 and H2AK119ub levels, RT-qPCR or RNA-seq to assess global transcriptomic changes, and chromatin immunoprecipitation (ChIP) to evaluate H3K27me3 occupancy at target loci. Cell-based phenotypic analyses such as CCK-8 proliferation assays, transwell migration/invasion, and flow cytometry for cell cycle and apoptosis provide direct readouts of CBX8-dependent tumor cell behavior. Additionally, the cells support co-immunoprecipitation studies to characterize PRC1 complex interactions and drug sensitivity screens with epigenetic inhibitors targeting EZH2 or other PRC2 components. For further information or to discuss custom applications, please contact Ascent Research.
