The KRT14 Knockout Ca Ski Polyclonal Cells are a CRISPR/Cas9-edited polyclonal population of Ca Ski cells carrying targeted disruptions in the KRT14 locus, generating a loss-of-function model for keratin 14. Supplied as a heterogeneous pool of edited cells, this product enables robust depletion of keratin 14 protein while maintaining genetic diversity suitable for pooled assays. It provides a powerful tool for dissecting intermediate filament biology and epithelial cell homeostasis.
The host Ca Ski cell line is an HPV-16 positive human cervical epidermoid carcinoma line originally isolated from a small intestine metastasis. These adherent epithelial cells retain integrated viral oncogenes E6 and E7, which deregulate p53 and Rb, making them a standard model for HPV-driven cervical cancer. The incorporation of KRT14 knockout in this background creates a relevant system for studying keratin cytoskeleton disruption in the context of HPV-mediated oncogenesis.
KRT14 encodes a type I intermediate filament protein that forms obligate heterodimers with keratin 5 (KRT5) to maintain epithelial structural integrity. The keratin network is tethered to desmosomes through interactions with DSP, JUP, PKP1, and PLEC. Transcription is regulated upstream by TP63. KRT14 knockout disrupts this scaffold, upregulating mesenchymal markers VIM, SNAI1, TWIST1, ZEB1, and matrix metalloproteinases MMP2 and MMP9, driving epithelial-to-mesenchymal transition and enhancing cell migration and invasion.
In Ca Ski cells, KRT14 loss synergizes with HPV oncoproteins to promote a more invasive phenotype, modeling cervical carcinoma progression and EMT. The polyclonal knockout population captures heterogeneous responses, enabling the study of intermediate filament collapse on cell adhesion, motility, and drug sensitivity. This model is well-suited for dissecting the interplay between viral transformation and keratin remodeling.
The product supports applications such as EMT and metastasis research, intermediate filament biology, and biomarker discovery. Representative assays include Western blot, immunofluorescence, RT-qPCR, wound healing, Transwell invasion, cell adhesion, flow cytometry for EMT markers, and RNA-seq for transcriptomic profiling. This knockout model serves as a valuable platform for mechanistic and translational research in epithelial cancers. For further information or to inquire about custom services, please contact Ascent Research.
