This KDM5C knockout product consists of a CRISPR/Cas9-edited polyclonal cell population derived from the human Ca Ski cervical carcinoma cell line. The polyclonal format ensures genetic heterogeneity typical of a knockout pool, minimizing clonal selection bias while providing a robust model for studying KDM5C loss-of-function. Using CRISPR/Cas9-mediated gene disruption, the KDM5C locus has been targeted to ablate functional KDM5C protein expression, enabling researchers to investigate the epigenetic consequences of KDM5C deficiency without relying on a single-cell-derived clone.
Ca Ski cells originate from a metastatic lesion in the small intestine of a patient with cervical epidermoid carcinoma and harbor an integrated HPV16 genome. These epithelial cells are widely employed as an in vitro model for HPV-positive cervical cancer, recapitulating key aspects of viral oncogenesis including expression of E6 and E7 oncoproteins. The Ca Ski line??s well-characterized karyotype and stable HPV16 integration provide a physiologically relevant background for dissecting host epigenetic regulators in the context of persistent HPV infection.
KDM5C encodes a histone demethylase specific for di- and tri-methylated H3K4 (H3K4me2/me3). By erasing these activating marks, KDM5C functions as a transcriptional repressor. It operates within a network of interacting partners including the REST/NRSF corepressor complex, SIN3A, and histone deacetylases (HDACs). Upstream regulation involves transcription factors such as MYC and REST, and post-translational modifications like ubiquitination and phosphorylation. Downstream, KDM5C influences chromatin at promoters controlling proliferation, differentiation, and tumor suppression; in cervical cancer, it may modulate expression of HPV oncogenes and host tumor suppressors.
In Ca Ski cells, knockout of KDM5C creates a powerful tool for investigating how histone demethylation impacts HPV-driven carcinogenesis. Given that KDM5C can act as either a tumor suppressor or an oncogene depending on cellular context, this polyclonal knockout model allows researchers to explore its dual roles in cervical cancer. By comparing wild-type Ca Ski cells with the KDM5C-disrupted population, scientists can assess changes in H3K4 methylation patterns, transcriptional programs of HPV and host genes, and phenotypic outcomes such as cell cycle progression, apoptosis, and invasive capacity. The model is particularly suited to studying crosstalk between epigenetic silencing mechanisms and viral oncogene expression.
Researchers can employ this knockout cell population in a variety of experimental workflows. Western blotting and immunofluorescence monitor global H3K4me3/me2 levels, while ChIP-qPCR quantifies histone modifications at specific promoters. RT-qPCR and RNA-seq reveal transcriptional changes downstream of KDM5C loss, including effects on HPV E6/E7 and host tumor suppressors. Functional assays such as proliferation, migration, and invasion, combined with drug sensitivity screening against epigenetic inhibitors, permit evaluation of therapeutic vulnerabilities. The KDM5C knockout Ca Ski polyclonal cells thus serve as a versatile platform for epigenetic cancer research and drug discovery. For further information, please contact Ascent Research.
