The KDM5C Knockout CAL-27 Polyclonal Cells consist of a CRISPR/Cas9-edited polyclonal knockout cell population derived from the human CAL-27 tongue squamous cell carcinoma line, with disruption of the KDM5C gene. This loss-of-function model facilitates investigation of KDM5C histone demethylase function in an oral cancer context. The polyclonal nature avoids clonal selection artifacts, preserving the epithelial and tumorigenic characteristics of the parental cells. Standard culture conditions are appropriate, with recommended verification of knockout efficiency.
The CAL-27 cell line is a well-characterized model of oral squamous cell carcinoma derived from a human tongue tumor. These adherent epithelial cells display cytokeratin expression and aberrant cell cycle regulation, commonly used in head and neck cancer research to study tumorigenesis, invasion, and therapeutic responses. Its genomic alterations reflective of human disease provide a relevant background for examining epigenetic regulators like KDM5C in epithelial cancers.
KDM5C is a histone H3K4 demethylase that removes methyl groups from H3K4me2/me3, acting as a transcriptional repressor. It forms a core component of the REST co-repressor complex and interacts with histone deacetylases. By modulating promoter H3K4 methylation, KDM5C regulates genes involved in neuronal development, cell cycle control, and tumor suppression. Upstream transcription factors and signaling pathways control its activity, while downstream targets exhibit altered expression upon changes in H3K4 methylation, depending on cellular context. The RB1 pathway is among the networks influenced by KDM5C-mediated epigenetic regulation.
In CAL-27 oral squamous carcinoma cells, KDM5C knockout disrupts the epigenetic landscape, enabling study of chromatin state alterations and gene expression changes in tumor biology. Loss of KDM5C-mediated repression via the REST complex and histone deacetylases may derepress genes promoting proliferation or blocking differentiation. This model links H3K4 hypermethylation to oral cancer phenotypes like growth, migration, and drug sensitivity. It also provides a platform for comparative cancer studies and X-linked intellectual disability research using neuronal differentiation.
Applications include ChIP-qPCR for H3K4me3 enrichment, Western blotting for histone modifications, RT-qPCR or RNA-seq for transcriptomic profiling, and functional assays like proliferation and migration. Immunofluorescence visualizes H3K4 methylation patterns. These cells support epigenetic regulation studies, oral cancer research, drug target validation, and neurodevelopmental disorder modeling. For further information or a quotation, contact Ascent Research.
