The KDM5B Knockout AGS Polyclonal Cells represent a CRISPR/Cas9-edited polyclonal knockout population with disruption of the KDM5B gene in the AGS human gastric epithelial cell line. This loss-of-function model enables investigation of KDM5B??s role in epigenetic regulation and gastric cancer biology without clonal selection, providing a heterogeneous pool suitable for functional studies.
The AGS cell line, derived from a gastric adenocarcinoma of a 54-year-old female, exhibits adherent epithelial morphology and retains features of gastric mucosal cells, including mucus secretion and barrier functions. It serves as a well-established model for gastric cancer research, particularly for studying genes implicated in tumorigenesis and mucosal biology.
KDM5B encodes a histone demethylase that removes methyl groups from H3K4me2/3, functioning as a transcriptional repressor by interacting with REST corepressor, PRC2, and HDAC1/2. Upstream, its expression is regulated by retinoic acid receptors (RARs), miR-137, and E2F transcription factors. KDM5B targets include CDKN1A (p21), HOX clusters, DAPK1, and RARB. Demethylation of H3K4me3 at promoters silences these genes, linking KDM5B to chromatin remodeling, retinoic acid signaling, and stem cell differentiation. In the retinoic acid pathway, RAR?? recruits KDM5B to mediate repression of target genes.
In gastric adenocarcinoma, KDM5B promotes proliferation and inhibits differentiation by epigenetically silencing tumor suppressors. This knockout model allows assessment of phenotypic changes upon KDM5B loss in AGS cells, enabling studies on cell proliferation, migration, and apoptosis. It is particularly useful for exploring the reversal of malignant traits and the role of KDM5B in maintaining an undifferentiated state through H3K4 demethylation.
Applications include functional genomics of histone demethylases, drug target validation, and epigenetic studies in gastric cancer. The cells support ChIP-qPCR, RNA-seq, RT-qPCR, Western blotting, and functional assays such as proliferation, apoptosis flow cytometry, and migration experiments. They provide a platform for investigating retinoic acid signaling and cancer stem cell biology. For further details, please contact Ascent Research.
