The HCFC1R1 Knockout Ca Ski Polyclonal Cells are a CRISPR/Cas9-edited mixed population of Ca Ski cells with targeted disruption of the HCFC1R1 gene. This polyclonal knockout model provides a heterogeneous cell pool for loss-of-function studies, avoiding clonal selection biases. It enables investigation of HCFC1R1-dependent processes in a human cervical carcinoma background, suitable for experiments requiring population-level gene inactivation.
Ca Ski cells are a human cervical carcinoma epithelial line isolated from a cervical metastasis. They contain integrated HPV-16 DNA and express E6/E7 oncoproteins, rendering them tumorigenic in mouse models. Widely used in cervical cancer research, Ca Ski cells retain epithelial characteristics and serve as a relevant model for HPV-driven oncogenesis and preclinical drug testing. Their viral etiology and epithelial origin provide a clinically pertinent context for studying gene functions in tumor development.
HCFC1R1 is a subunit of the SET1/COMPASS histone methyltransferase complex that trimethylates histone H3 at lysine 4 (H3K4me3) at gene promoters, promoting RNA polymerase II transcription. It interacts with HCF-1 and ZFP91 to anchor the complex to chromatin, and also associates with mRNA capping enzyme, linking transcription to mRNA processing. Core complex members include ASH2L, RBBP5, DPY30, WDR5, and catalytic subunits SETD1A/B. By regulating H3K4me3, HCFC1R1 influences transcriptional programs critical for cell growth and identity. Its disruption can alter histone modification patterns and gene expression networks.
In Ca Ski cells, loss of HCFC1R1 offers a powerful tool to examine its contribution to HPV-mediated transformation. Since HPV oncoproteins hijack host transcription, HCFC1R1 may be involved in maintaining oncogenic gene expression programs via epigenetic regulation. This model allows dissection of SET1/COMPASS complex functions in cervical carcinoma, potentially revealing how H3K4me3-dependent transcription supports tumorigenic phenotypes and identifying epigenetic dependencies for therapeutic targeting.
Applications include Western blot for HCFC1R1 and histone modifications, RT-qPCR and RNA-seq for transcriptomic changes, and ChIP-qPCR for H3K4me3 occupancy. Functional assays assess proliferation, apoptosis, migration, and invasion, while drug sensitivity screens test epigenetic inhibitors. These polyclonal knockout cells provide a versatile platform for investigating the role of HCFC1R1 in cervical cancer biology and transcriptional regulation. For additional information or customized services, please contact Ascent Research.
