The KDM5C Knockout NCI-H1703 Polyclonal Cells consist of a CRISPR/Cas9-edited polyclonal population of NCI-H1703 human lung squamous cell carcinoma cells with disruption of the KDM5C gene. This pooled knockout model retains genetic diversity while eliminating functional KDM5C expression, enabling loss-of-function studies in an epigenetically relevant background.
NCI-H1703 is a lung squamous cell carcinoma cell line established from a 54-year-old male smoker. Exhibiting epithelial morphology, it is a well-characterized model for non-small cell lung cancer research, particularly of the squamous subtype. The line carries smoking-associated mutations and maintains key oncogenic signaling pathways, providing a suitable context to study chromatin modifiers such as KDM5C.
KDM5C (JARID1C) is a histone H3 lysine 4 (H3K4) demethylase that removes di- and trimethyl groups, functioning as a transcriptional repressor. It operates in repressive complexes with SIN3A, HDAC1/2, REST, and CoREST, and interacts with polycomb repressive complex 2 components. Upstream regulators include RB1, REST, hypoxia-inducible factors, E2F transcription factors, and miR-137. KDM5C-mediated demethylation at promoters silences target genes such as CDH1 (E-cadherin), CCND1 (Cyclin D1), and CDKN1A (p21), thereby controlling epithelial differentiation, cell cycle progression, and tumor suppression.
In NCI-H1703 lung carcinoma cells, loss of KDM5C disrupts the H3K4 methylation landscape, likely leading to derepression of E-cadherin, Cyclin D1, and p21. This may promote an epithelial?Cmesenchymal transition-like phenotype, alter proliferation rates, and affect cell cycle checkpoints. Consequently, the knockout model is valuable for dissecting KDM5C-dependent epigenetic regulation in squamous lung cancer and for studying how the KDM5C-REST-SIN3A axis modulates tumor aggressiveness.
Typical applications include ChIP-qPCR for H3K4me3 profiling, RNA-seq transcriptomics, RT-qPCR and western blotting for target validation, and functional assays such as proliferation, migration, and invasion studies. The polyclonal knockout cells are also suited for drug sensitivity screens and co-immunoprecipitation to interrogate altered protein interaction networks. This tool addresses research on epigenetic cancer mechanisms, chromatin remodeling in lung squamous carcinoma, and KDM5C-associated disorders including X-linked intellectual disability and Claes-Jensen syndrome. For further information, please contact Ascent Research.
