KAT7 Knockout HGC-27 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population featuring targeted disruption of the KAT7 (HBO1) gene in the HGC-27 human gastric cancer cell line. This heterogeneous pool retains diverse editing events, enabling robust loss-of-function studies without clonal bias. Ideal for investigating KAT7??s roles in histone acetylation, cell cycle regulation, and gastric cancer biology. The product provides a versatile genetic tool for dissecting gene function in a disease-relevant background.
HGC-27 is a poorly differentiated human gastric adenocarcinoma cell line, widely used as a model for gastric cancer research. Its aggressive growth phenotype and epithelial origin make it suitable for probing molecular drivers of gastric tumorigenesis, including epigenetic regulators. KAT7 knockout in this context allows evaluation of proliferation, chromatin remodeling, and therapeutic sensitivity.
KAT7 (HBO1) is a histone acetyltransferase that acetylates histone H4 at lysines 5, 8, and 12 (H4K5/8/12ac), a key step in DNA replication licensing. Activated by CDK2/Cyclin A phosphorylation and CDT1, KAT7 associates with ING4/5, JADE1/2/3, and EAF6 scaffold proteins at replication origins. This acetylation facilitates MCM2-7 helicase loading and S-phase entry. KAT7 also transcriptionally regulates cell cycle genes, linking epigenetic modulation to proliferation. Downstream, it promotes PCNA-mediated replication and coordinates with ORC1 and CDT1 for origin firing. Additionally, KAT7-mediated H4 acetylation influences chromatin remodeling and gene expression beyond replication origins.
In gastric cancer, KAT7 dysregulation contributes to oncogenic proliferation through aberrant histone acetylation and unchecked replication licensing. This polyclonal knockout model enables dissection of KAT7-dependent epigenetic and cell cycle mechanisms within a gastric adenocarcinoma context. Loss of KAT7 is expected to reduce H4 acetylation, impair MCM loading, and block cell cycle progression, uncovering vulnerabilities. The model thus serves as a powerful tool for studying KAT7??s role in gastric cancer and for testing targeted therapies aimed at KAT7 or its interacting partners.
Typical applications include MTT and colony formation proliferation assays, cell cycle analysis by flow cytometry, EdU incorporation for S-phase entry, ChIP-qPCR of H4K8ac at replication origins, and RNA-seq transcriptomics. Western blotting confirms KAT7 loss and histone acetylation changes. Drug sensitivity testing, e.g., cisplatin response, evaluates chemoresistance links. Migration and invasion assays assess metastatic potential. This versatile knockout population supports comprehensive functional genomics in gastric cancer research, facilitating study of epigenetic mechanisms and therapeutic resistance. For further details, please contact Ascent Research.
