The KDM5C Knockout KYSE-150 Polyclonal Cells represent a CRISPR/Cas9-edited polyclonal cell population designed for loss-of-function studies of the KDM5C gene in a human esophageal squamous cell carcinoma (ESCC) background. This product consists of a heterogeneous pool of KYSE-150 cells harboring targeted disruptions of the KDM5C locus, enabling robust investigation of KDM5C-dependent phenotypes without clonal selection biases. As a polyclonal knockout, it captures the diversity of editing outcomes across the cell population, making it suitable for population-level functional genomics and epigenetic profiling.
The host cell line, KYSE-150, is derived from a poorly differentiated esophageal squamous cell carcinoma of a Japanese female and serves as a widely used model for ESCC biology. KYSE-150 cells retain key features of esophageal epithelial cells and exhibit hallmark properties of malignant transformation, including aberrant signaling and chromatin states. This background provides a clinically relevant platform to dissect the epigenetic mechanisms underpinning esophageal carcinogenesis and to test therapeutic interventions.
KDM5C encodes a JmjC-domain-containing histone demethylase that specifically removes di- and tri-methyl groups from lysine 4 of histone H3 (H3K4me2/me3), acting as a transcriptional repressor. It functions within multi-protein complexes that include HDAC1, HDAC2, REST (RE1-silencing transcription factor), RCOR1, and SIN3A, coupling histone deacetylation and demethylation to enforce gene silencing. KDM5C activity is regulated by upstream transcriptional programs and microRNA-mediated control, and it opposes the action of MLL family histone methyltransferases. Downstream, KDM5C modulates the expression of Notch target genes and other genes involved in cell proliferation and differentiation, thereby influencing key cellular decisions.
In the context of ESCC, KDM5C has been implicated as a tumor suppressor, with loss-of-function potentially contributing to oncogenic progression through derepression of growth-promoting genes or disruption of differentiation programs. CRISPR-mediated knockout in KYSE-150 cells provides a clean genetic background to delineate KDM5C??s role in maintaining the esophageal epithelial transcriptome and to identify its direct and indirect targets in cancer cells. This model allows researchers to discriminate between KDM5C-dependent and -independent effects on chromatin structure and gene expression under various experimental conditions.
Typical applications include quantitative assessment of global and locus-specific H3K4 methylation by western blotting and ChIP-qPCR, expression profiling of target genes via RT-qPCR or RNA-seq, and functional assays such as proliferation, apoptosis, migration, invasion, and drug sensitivity analyses. These polyclonal knockout cells are particularly valuable for epigenetic drug screening and for exploring combinatorial effects with histone deacetylase inhibitors or other chromatin-modifying agents. For further information or customized services, please contact Ascent Research.
