The KDM5C Knockout KYSE-30 Polyclonal Cells represent a CRISPR/Cas9-edited polyclonal population derived from the human esophageal squamous cell carcinoma line KYSE-30, engineered for loss-of-function interrogation of KDM5C. This gene-disrupted pool preserves cellular heterogeneity, providing a robust model for studying KDM5C-dependent phenotypes without clonal artifacts. The product is formatted as frozen polyclonal knockout cells, ready for immediate use in a wide spectrum of epigenetic and oncology applications.
KYSE-30 is a well-differentiated human esophageal squamous cell carcinoma line originally established from an invasive tumor resected from a 64-year-old Japanese male. This cell line retains many hallmarks of esophageal cancer, including activated oncogenic signaling and aberrant chromatin landscapes, making it an ideal host for assessing the impact of KDM5C loss in a disease-relevant setting. The KYSE-30 background offers a clinically pertinent framework for linking epigenetic changes to cancer progression.
KDM5C is a histone H3K4me2/me3 demethylase that functions as a potent transcriptional repressor. It catalyzes the removal of activating methyl marks from histone H3, thereby condensing chromatin and silencing genes involved in cell cycle control and neuronal specification. KDM5C is recruited to target loci through direct associations with the REST corepressor complex, including HDAC1, HDAC2, and SIN3A, and cooperates with the RB1/E2F pathway to repress CDKN1A and HOX gene clusters. Its activity is regulated upstream by E2F transcription factors, retinoic acid, MYC, and various microRNAs, placing it at a central node of epigenetic and proliferative control.
Within esophageal squamous cell carcinoma, KDM5C is believed to act as a tumor suppressor, and its ablation in KYSE-30 cells derepresses oncogenic programs governed by H3K4me3. The resulting polyclonal knockout model allows researchers to probe how KDM5C orchestrates global H3K4 methylation patterns, modulates gene expression signatures, and influences malignant behavior. This system is particularly suited for evaluating epigenetic drug targets and the interplay between histone demethylation and other chromatin regulators in esophageal carcinogenesis.
Applications of these knockout cells encompass functional characterization of histone modifiers, high-throughput epigenetic drug screening, and CRISPR-based knockout validation. Standard experimental workflows include immunoblotting for KDM5C, quantitative H3K4me3 level assessment, RT-qPCR for CDKN1A and HOX genes, and ChIP-qPCR or ChIP-seq. Growth assays, cell cycle analysis, and HDAC inhibitor sensitivity testing can evaluate KDM5C-dependent phenotypes. RNA-seq provides transcriptomic insights. Contact Ascent Research for technical inquiries, custom orders, or collaborative development.
