The CBX5 Knockout HGC-27 Polyclonal Cells represent a CRISPR/Cas9-mediated gene-disrupted cell population, designed as a loss-of-function model for studying the epigenetic regulator CBX5. This product consists of a heterogeneous pool of HGC-27 cells that have undergone targeted disruption of the CBX5 locus via CRISPR/Cas9 ribonucleoprotein delivery, generating a polyclonal knockout population. The use of a polyclonal format enables researchers to assess gene function in a setting that mirrors the natural variability of engineered cellular populations, circumventing the clonal selection biases associated with single-cell-derived lines. This model is provided as a ready-to-use tool for functional genomics, chromatin biology, and cancer research, without requiring end-users to perform gene editing or selection steps.
The host cell line, HGC-27, is an epithelial cell line established from a lymph node metastasis of a human undifferentiated gastric adenocarcinoma. This cell line exhibits aggressive growth and invasive properties, making it a widely used system for investigating the molecular mechanisms of gastric cancer progression, metastasis, and drug response. Its genetic background, characterized by alterations in pathways such as Wnt/??-catenin and TGF-??, provides a clinically relevant context for studying the interplay between epigenetic silencing and oncogenic signaling.
CBX5 encodes heterochromatin protein 1 alpha (HP1??), a chromodomain-containing reader of trimethylated lysine 9 on histone H3 (H3K9me3). Through this interaction, HP1?? recruits chromatin-modifying complexes??including HDAC1/2, DNMT1, and CoREST??to establish and maintain heterochromatic regions, leading to transcriptional repression of target genes. The activity of CBX5 is regulated by upstream kinases such as Aurora B and PLK1, by transcription factors like E2F1, and by signaling pathways including TGF-?? and p53. Its downstream targets comprise cell cycle regulators (CDKN1A, CCND1), epithelial-mesenchymal transition markers (CDH1, VIM), and repetitive elements (LINE-1 retrotransposons). Key interacting partners include SUV39H1 (the major H3K9 methyltransferase), Lamin B, CAF-1, TIF1??, and EZH2, placing CBX5 at the nexus of chromatin organization, epigenetic silencing, and genome stability.
In the HGC-27 gastric adenocarcinoma model, CBX5 knockout disrupts HP1??-mediated gene silencing, leading to de-repression of tumor-suppressive loci such as CDKN1A and CDH1. This molecular alteration impairs cell proliferation, migration, and invasion, largely due to the re-establishment of growth-inhibitory and adhesive programs. Consequently, this polyclonal knockout system offers a physiologically relevant platform to dissect how aberrant heterochromatin maintenance contributes to the malignant phenotype of gastric cancer. It also permits cross-comparison with other CBX5-dependent cancer types, including breast, hepatocellular, and colorectal carcinomas, where HP1?? overexpression has been linked to poor prognosis and therapeutic resistance.
This product is suitable for a broad range of advanced research applications, including the study of epigenetic regulation of tumor suppressors, mechanistic dissection of Wnt/??-catenin pathway crosstalk with chromatin modifiers, and validation of small-molecule inhibitors targeting heterochromatin components. Typical experimental readouts encompass chromatin immunoprecipitation sequencing (ChIP-seq) to map H3K9me3 landscapes, RT-qPCR and Western blotting for downstream target expression, immunofluorescence to assess HP1?? localization, and functional assays such as colony formation, transwell migration/invasion, and flow cytometric cell cycle analysis. The polyclonal knockout cells can also be employed in drug sensitivity screens to identify compounds that synergize with epigenetic reactivation. For further information, please contact Ascent Research.
