CBX3 Knockout HGC-27 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout population originating from the HGC-27 human gastric carcinoma cell line, featuring disruption of the CBX3 gene encoding heterochromatin protein 1 gamma (HP1??). This polyclonal knockout model provides a heterogeneous cell pool that avoids clonal bias and is suitable for studying HP1?? loss-of-function effects in cancer-relevant contexts.
The HGC-27 cell line was derived from a lymph node metastasis of a poorly differentiated gastric adenocarcinoma, representing an aggressive model for gastric cancer research. HGC-27 cells are extensively characterized for their metastatic properties, genetic alterations, and responses to anticancer agents, making them a valuable host for epigenetic knockout studies.
CBX3/HP1?? is a conserved heterochromatin protein that specifically binds trimethylated histone H3 lysine 9 (H3K9me3) via its chromodomain. The H3K9me3 mark is deposited by upstream methyltransferases SUV39H1 and SETDB1, and HP1?? binding is regulated by Aurora B kinase-mediated phosphorylation. Once bound, HP1?? recruits or interacts with the Lamin B receptor, histone deacetylases (HDACs), proliferating cell nuclear antigen (PCNA), and chromatin assembly factor 1 (CAF-1) to orchestrate chromatin compaction and gene silencing. These interactions contribute to heterochromatin formation, centromeric cohesion, DNA repair, and cell cycle regulation, thereby maintaining genome stability.
In gastric carcinoma, perturbations in heterochromatin maintenance are linked to genomic instability and metastatic progression. Knocking out CBX3 in HGC-27 cells can disrupt heterochromatin organization, potentially derepressing silenced tumor suppressor genes or affecting DNA repair pathways. This model is especially pertinent for investigating the epigenetic underpinnings of poorly differentiated, metastatic gastric cancers and for identifying vulnerabilities that could be exploited therapeutically.
This polyclonal knockout cell product supports a range of assays. Western blotting confirms HP1?? protein depletion. RT-qPCR quantifies changes in expression of heterochromatin-regulated genes. ChIP-qPCR for H3K9me3 reveals altered histone modification landscapes. Immunofluorescence visualizes HP1?? localization and nuclear architecture. Functional assays, including proliferation, migration, and invasion, assess phenotypic consequences. Drug sensitivity testing can evaluate responses to epigenetic inhibitors. For additional information, please contact Ascent Research.
