The KAT7 Knockout CAL-27 Polyclonal Cells product constitutes a CRISPR/Cas9-edited polyclonal knockout cell population generated from the CAL-27 human tongue squamous cell carcinoma cell line. This loss-of-function model disrupts the KAT7 gene (also known as HBO1), which encodes a MYST-type histone acetyltransferase. The polyclonal knockout cells are provided as a mixed population, enabling pooled analysis of target gene disruption without single-cell cloning. Designed for rigorous biomedical research, this reagent is suitable for studying the functional consequences of KAT7 ablation in an oral cancer context.
The parental CAL-27 cell line is derived from a human tongue squamous cell carcinoma and serves as a widely used model for oral squamous cell carcinoma (OSCC). These epithelial cells retain characteristic features of malignant transformation, including dysregulated proliferation, altered chromatin state, and aberrant DNA replication control. CAL-27 cells are extensively employed to explore OSCC biology, drug response, and metastatic behavior, making them a relevant host for interrogating epigenetic regulators such as KAT7.
KAT7 (HBO1) functions as a histone acetyltransferase that catalyzes acetylation of histone H4 at lysines 5, 8, and 12, as well as H3K14, thereby influencing chromatin structure and genome stability. Its enzymatic activity is regulated by upstream signals including CDK kinases, the ATM/ATR DNA damage response kinases, and replication licensing factors Cdt1 and geminin. KAT7 operates within macromolecular complexes containing JADE family proteins, ING4/5, BRPF1/2/3, and EAF6. Downstream, KAT7-mediated acetylation promotes loading of the MCM2-7 helicase complex at replication origins, facilitating DNA replication licensing. It also acetylates p53, modulating transcriptional activation and DNA repair pathway choice. Through these interactions, KAT7 couples cell cycle progression to chromatin dynamics and maintains genome integrity under replication stress.
In the context of oral squamous cell carcinoma, KAT7 is implicated in sustaining proliferative capacity and epigenetic reprogramming. Dysregulation of KAT7 activity may contribute to oncogenesis by altering replication origin firing and gene expression programs. The CAL-27 knockout model enables the dissection of KAT7-dependent mechanisms that support OSCC cell growth, survival, and response to genotoxic agents. Given that KAT7 interfaces with critical regulators like p53 and the MCM complex, this system provides a platform to investigate how histone acetylation integrates with DNA replication and DNA damage signaling in cancer cells.
Typical research applications include mechanistic studies on DNA replication stress, epigenetic regulation of gene expression, and chromatin remodeling in oral cancer. This polyclonal KO product can be used in western blotting to assess changes in histone H4K5/8/12 acetylation, ChIP-qPCR for histone marks at specific loci, RT-qPCR for downstream target genes, DNA fiber assays to monitor replication fork dynamics, flow cytometry for cell cycle analysis, and proliferation or drug sensitivity assays. Additionally, RNA-seq experiments may reveal transcriptome-wide alterations upon KAT7 loss. For further information, please contact Ascent Research.
