The CBX3 knockout AGS polyclonal cells are a CRISPR/Cas9-edited polyclonal knockout cell population targeting the CBX3 gene in the AGS gastric adenocarcinoma cell line. This product provides a heterogeneous mixture of cells with disrupted CBX3 alleles, enabling loss-of-function studies without clonal selection. The polyclonal format ensures representation of diverse genetic backgrounds, minimizing clonal artifacts and facilitating robust functional analyses of CBX3-dependent processes.
The AGS cell line, derived from a Caucasian female patient with gastric adenocarcinoma, is a widely used epithelial model for gastric cancer research. These cells retain key characteristics of gastric epithelium and exhibit anchorage-independent growth, making them suitable for investigating tumor biology, drug responses, and signalling pathways implicated in gastric carcinogenesis. AGS cells are particularly valuable for studying epigenetic mechanisms due to their well-characterized chromatin landscape and responsiveness to microenvironmental cues.
CBX3 (HP1??) is a chromobox family protein that binds histone H3 trimethylated at lysine 9 (H3K9me3) via its chromodomain, functioning as a central component of heterochromatin-mediated gene silencing. It interacts with the SUV39H1/2 methyltransferases, which establish the H3K9me3 mark, and with other HP1 family members (CBX1, CBX5) and the Lamin B receptor to maintain condensed chromatin states. CBX3 represses transcription of downstream targets including CDKN1A (p21) and E2F-regulated genes, thereby modulating cell cycle progression and senescence. Dysregulation of this network is implicated in oncogenic transformation and epigenetic reprogramming.
In the context of gastric adenocarcinoma, CBX3 overexpression has been correlated with advanced disease and poor prognosis, potentially through silencing of tumor suppressor loci and escape from senescence. Disruption of CBX3 in AGS polyclonal cells enables dissection of its role in maintaining the transformed phenotype, epigenetic regulation of proliferation, and senescence induction. This model is particularly relevant for investigating the interplay between H3K9me3-mediated heterochromatin and tumor suppressors like p21, as well as for evaluating epigenetic therapies targeting SUV39H1 or heterochromatin integrity.
Researchers can employ this knockout cell population in diverse assays, including chromatin immunoprecipitation coupled with quantitative PCR (ChIP-qPCR) to assess H3K9me3 enrichment at specific loci, western blotting to monitor protein-level changes in CBX3 and its interacting partners, and senescence-associated ??-galactosidase staining to quantify cellular senescence. Proliferation assays and transcriptomic profiling by RNA-seq further support the exploration of CBX3-dependent transcriptional programs. For further information on this product or to inquire about additional gene-edited models, please contact Ascent Research.
