The KAT7 Knockout SK-OV-3 Polyclonal Cells consist of a CRISPR/Cas9-edited polyclonal population of human SK-OV-3 ovarian adenocarcinoma cells with targeted disruption of the KAT7 gene. This heterogeneous cell pool, generated without clonal selection, provides a loss-of-function model to study KAT7-dependent histone acetyltransferase activity and related signaling in a cancer-relevant system. It is well-suited for functional genomics and drug discovery applications in ovarian cancer research.
The SK-OV-3 host cell line is a human ovarian adenocarcinoma epithelial line derived from metastatic ascitic fluid. It exhibits p53-null status and HER2/neu (ERBB2) overexpression, representing high-grade serous ovarian carcinoma. These cells are tumorigenic in immunocompromised mice and display genomic instability, making them an appropriate model for investigating oncogenic mechanisms and epigenetic regulation. The genetic background of SK-OV-3 provides a clinically relevant context for examining KAT7??s contributions to ovarian tumor biology.
KAT7 (HBO1) is a MYST-family histone acetyltransferase that acetylates histone H3 at lysine 14 (H3K14ac) and histone H4 at lysines 5, 8, and 12 (H4K5/K8/K12ac). It acts in multiprotein complexes with JADE1/2/3 scaffolds, ING4/5 tumor suppressors, and BRPF1/2/3. Upstream, KAT7 is regulated by CDK1?Ccyclin B and JADE family proteins, while downstream, it promotes transcription of MYC and CCND1 through Wnt signaling and facilitates DNA replication licensing by priming MCM2-7 helicase loading via interactions with CDT1 and ORC1. Thus, KAT7 bridges chromatin modification with gene expression and genome duplication.
In high-grade serous ovarian cancer, KAT7 dysregulation may drive oncogenic transcription and contribute to replication stress responses. The SK-OV-3 model, lacking p53, allows assessment of KAT7-dependent proliferation and survival mechanisms, particularly the interplay with HER2 signaling. Disrupting KAT7 in these cells can reveal vulnerabilities related to Wnt pathway activation and replication licensing defects, offering insights into therapeutic strategies that target epigenetic regulators in ovarian cancer.
This polyclonal knockout model supports diverse assays: western blotting for H3K14ac/H4K5ac, RT-qPCR for MYC/CCND1, ChIP for origin binding, EdU/PI cell cycle analysis, DNA fiber assays for replication dynamics, and colony formation/apoptosis assays. It is suitable for epigenetic inhibitor screening and synthetic lethality studies. For further technical details or to inquire about customization, please contact Ascent Research.
