The KRT7 Knockout Ca Ski Polyclonal Cells constitute a CRISPR/Cas9-edited polyclonal population derived from the Ca Ski human cervical carcinoma cell line, engineered for loss-of-function studies of the KRT7 gene. This product provides a versatile knockout model with a genetically heterogeneous pool of cells, each carrying CRISPR/Cas9-mediated disruption of the KRT7 locus, enabling robust functional genomics analyses.
The Ca Ski host cell line is an adherent epithelial cell line established from a human cervical squamous cell carcinoma metastasis. These cells harbor an integrated human papillomavirus type 16 (HPV-16) genome and constitutively express the viral E6 and E7 oncoproteins, which inactivate the tumor suppressors p53 and retinoblastoma protein (Rb), respectively. This genetic background recapitulates key oncogenic drivers of HPV-positive cervical cancers, making Ca Ski a well-characterized model for studying cervical carcinogenesis and therapeutic responses.
KRT7 encodes keratin 7, a type II intermediate filament protein that pairs with type I keratins such as KRT18 to form heteropolymeric filaments essential for maintaining epithelial cytoarchitecture. KRT7 expression is regulated by transcription factors including TP63, JUN, FOS, and ETS1, and is responsive to estrogen receptor signaling. The keratin 7 network interacts with desmoplakin and plakoglobin, linking intermediate filaments to desmosomal junctions, and associates with integrin ??6??4 at hemidesmosomes. KRT7 also participates in signaling complexes involving 14-3-3 adaptor proteins, thereby influencing cell adhesion, migration, and intracellular signal transduction. Disruption of this network is known to impact cytoskeletal organization and epithelial-to-mesenchymal transition (EMT) dynamics.
In the Ca Ski cervical carcinoma background, KRT7 knockout dismantles the keratin intermediate filament scaffold, thereby compromising mechanical stability and altering the organization of cell?Cmatrix and cell?Ccell adhesion complexes. The loss of KRT7-driven filament networks interferes with the integration of signals from integrin-based adhesions and desmosomes, leading to changes in cellular stiffness, motility, and invasive behavior. Because Ca Ski cells express HPV-16 E6 and E7 oncoproteins, which already reprogram epithelial homeostasis, the ablation of KRT7 provides a unique system to interrogate how cytoskeletal disruption cooperates with viral oncogene-induced signaling in driving EMT and metastatic progression.
Researchers can employ these polyclonal KRT7 knockout Ca Ski cells in a wide range of assays to dissect the roles of keratin intermediate filaments in cervical cancer. Typical applications include monitoring EMT marker expression via RT-qPCR and western blotting, assessing cell migration through wound-healing assays, and evaluating invasive capacity using transwell invasion chambers. Immunofluorescence microscopy can visualize the collapse of keratin networks, while co-immunoprecipitation and RNA-sequencing enable the identification of altered KRT7 binding partners and downstream transcriptomic changes. Cytotoxicity and viability assays, such as MTT, facilitate drug resistance screening in the absence of KRT7. For further information and ordering details, please contact Ascent Research.
