The KDM5D Knockout AGS Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population originating from the AGS human gastric adenocarcinoma cell line. This product disrupts the Y-chromosome-linked histone demethylase KDM5D (JARID1D), creating a loss-of-function model in an epithelial gastric cancer background. The polyclonal composition minimizes clonal artifacts and maintains genetic diversity, making the population suitable for pooled epigenomic and functional analyses.
The parental AGS cell line, originally isolated from a female patient with gastric adenocarcinoma, exhibits adherent epithelial morphology and is widely used in gastrointestinal cancer research. These cells recapitulate key features of gastric carcinogenesis, including aberrant signaling and epigenetic dysregulation. As KDM5D is Y-chromosome-linked, the female origin ensures absence of endogenous protein, offering a clean background for exogenous expression and knockout analysis. This enables dissection of KDM5D-dependent chromatin and transcriptional programs without endogenous interference.
KDM5D is a histone demethylase that specifically removes methyl groups from H3K4me1/me2/me3, acting as a transcriptional repressor. It modulates downstream targets including HOX genes, cell cycle regulators, and tumor suppressors. KDM5D is regulated by upstream factors such as the androgen receptor, transcription factors, and miRNAs. The protein interacts with the androgen receptor, RB1, the NuRD complex, and HDACs, thereby linking histone demethylation to chromatin remodeling and androgen receptor signaling pathways that influence cell cycle progression.
In AGS gastric adenocarcinoma cells, KDM5D knockout enables study of epigenetic reprogramming. Loss of H3K4 demethylation is anticipated to alter global and locus-specific methylation, derepressing target genes. This model can probe effects on proliferation, migration, invasion, and epigenetic drug sensitivity. Because AGS cells lack endogenous KDM5D, this system uniquely isolates KDM5D-specific functions in a female gastric cancer context, circumventing confounding Y-chromosome influences.
Typical applications include western blotting for KDM5D and H3K4 methylation, RT-qPCR for target gene expression, and ChIP-qPCR for H3K4me3 occupancy. Functional assays assess proliferation, apoptosis, migration, and invasion. Drug sensitivity screens with epigenetic inhibitors (e.g., HDAC inhibitors) can validate therapeutic potential. For further details and technical support, contact Ascent Research.
