The KAT7 Knockout Ca Ski Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population designed to disrupt the KAT7 gene in the human Ca Ski cervical carcinoma cell line. This product provides a heterogeneous pool of cells with targeted gene disruption, enabling robust loss-of-function analysis of KAT7 in a well-characterized oncogenic background. The polyclonal format mirrors the genetic diversity of tumor cell populations, offering a relevant system for functional studies.
Ca Ski is an adherent epithelial cell line derived from a metastatic site of a human cervical carcinoma. These cells are persistently infected with human papillomavirus type 16 (HPV-16) and constitutively express the viral E6 and E7 oncoproteins, which inactivate the tumor suppressors p53 and Rb, respectively. This oncogenic background recapitulates key features of HPV-associated cervical cancers, including deregulated proliferation, and is widely used to study viral carcinogenesis.
KAT7 (HBO1) is a MYST-family histone acetyltransferase that acetylates histone H4 at K5, K8, and K12 and histone H3 at K14. Its activity is regulated by CDK1/cyclin B and CDK2/cyclin A phosphorylation, growth factor signaling (EGF, FGF), and transcription factors E2F and MYC. In Ca Ski cells, HPV E6/E7 oncoproteins further influence KAT7 function. KAT7 forms complexes with ING4/5, EAF6, and BRPF1/2/3 and interacts with ORC1 to facilitate MCM2-7 helicase loading at replication origins. KAT7-driven H4 acetylation promotes replication licensing, while H3 acetylation at promoters activates transcription of targets like MYC and CCND1. Additionally, KAT7 acetylates p53, modulating its activity. Thus, KAT7 couples chromatin modification to DNA replication initiation, cell cycle progression, and gene expression.
In the Ca Ski model, KAT7 constitutes a critical epigenetic regulator that integrates viral oncoprotein signals with chromatin dynamics. The functional loss of p53 and Rb due to E6/E7 creates a cellular context dependent on alternative pathways, where KAT7-mediated histone acetylation may sustain replication and transcription of oncogenic programs. Disrupting KAT7 allows investigation of how acetylation-controlled chromatin states contribute to cervical cancer cell proliferation, replication stress, and transcriptional addiction. This model is also relevant for probing acetyltransferase functions linked to developmental disorders and genome stability.
This polyclonal knockout system is compatible with diverse experimental workflows. Researchers can employ western blotting and RT-qPCR to confirm KAT7 loss and assess histone H4 acetylation and target gene expression (e.g., MYC, CCND1). Chromatin immunoprecipitation (ChIP) enables mapping of KAT7-dependent histone modification patterns, while DNA fiber assays and cell cycle flow cytometry evaluate replication dynamics and cell cycle distribution. EdU incorporation quantifies proliferation, and migration/invasion assays probe metastatic potential. Drug sensitivity screens, particularly with HDAC inhibitors, can identify epigenetic vulnerabilities in HPV-positive cervical cancer. RNA-seq transcriptomics can reveal global gene expression changes upon KAT7 disruption. For technical inquiries, please contact Ascent Research.
