The KAT7 Knockout SK-HEP-1 Polyclonal Cells represent a CRISPR/Cas9-edited polyclonal knockout cell population derived from the human hepatocellular carcinoma cell line SK-HEP-1. This product features targeted disruption of the KAT7 gene (also known as MYST2 or HBO1), which encodes a histone acetyltransferase critical for DNA replication licensing and epigenetic regulation. The polyclonal format provides a heterogeneous pool of edited cells, reflecting a range of loss-of-function alleles without clonal selection, thereby enabling robust functional studies that account for population-level effects. The knockout model serves as a valuable tool for dissecting the roles of KAT7 in cell cycle progression, chromatin dynamics, and tumor biology.
SK-HEP-1 is a well-established human liver adenocarcinoma cell line with epithelial morphology, originally isolated from the ascitic fluid of a patient with hepatocellular carcinoma. These cells express alpha-fetoprotein (AFP) and cytokeratins, markers indicative of their hepatic origin, and are widely utilized as a model system for investigating hepatocellular carcinoma pathogenesis, metastatic behavior, and drug sensitivity. The SK-HEP-1 background is particularly suited for exploring the molecular mechanisms underlying liver cancer, given its retention of key signaling pathways and its amenability to genetic manipulation and cell-based assays.
KAT7 functions as a histone acetyltransferase that acetylates histones H3 and H4, notably at H3 lysine 14 (H3K14) and H4 lysines 5, 8, and 12, thereby regulating chromatin accessibility and origin licensing. Its activity is modulated through interactions with the scaffolding proteins ING5, BRPF1, and JADE1, as well as cofactors such as EAF6 and MEAF6. KAT7 is recruited to replication origins via its interaction with CDT1, and its acetyltransferase activity promotes the loading of the MCM2-7 helicase complex, a process essential for DNA replication initiation. Upstream, KAT7 is regulated by cell cycle kinases including CDK2 and the transcription factor E2F1, while the replication inhibitor geminin (GMNN) provides negative regulation. Additionally, KAT7 intersects with the p53 pathway, contributing to tumor-suppressive functions under stress conditions. Through these interactions, KAT7 orchestrates critical checkpoints in cell cycle progression and gene expression.
In the context of SK-HEP-1 hepatocellular carcinoma cells, disruption of KAT7 offers a powerful model to elucidate the epigenetic mechanisms driving liver cancer. Aberrant histone acetylation patterns are commonly observed in HCC, and KAT7??s role in origin licensing and cell cycle control implicates it in malignant proliferation. Loss of KAT7 function may impair proper DNA replication and dysregulate downstream effectors such as CCND1 and CDK1, while also altering p53-dependent responses. Therefore, this polyclonal knockout population provides a physiologically relevant platform to study how KAT7-dependent chromatin modifications influence hepatocellular carcinoma progression and sensitivity to therapeutic agents. It enables researchers to investigate the interplay between epigenetic regulation and oncogenic signaling in a liver-specific cellular environment.
This knockout product is ideally suited for a broad spectrum of research applications. It can be employed in functional genomics studies investigating epigenetic control of DNA replication and cell cycle regulation in hepatocellular carcinoma. Researchers can utilize representative assays such as Western blotting for histone acetylation marks (e.g., H3K14ac, H4K5ac), chromatin immunoprecipitation followed by quantitative PCR (ChIP-qPCR) to assess KAT7 occupancy at replication origins, and flow cytometry to analyze cell cycle distribution. The model also facilitates drug target validation for KAT7 inhibitors, colony formation assays to evaluate tumorigenicity, and co-immunoprecipitation experiments to probe KAT7-containing protein complexes. Additional applications include RNA-seq-based transcriptomic profiling and immunofluorescence-based monitoring of MCM complex loading. For further information, please contact Ascent Research.
