The KAT7 Knockout KYSE-150 Polyclonal Cells product provides a CRISPR/Cas9-edited polyclonal knockout cell population for functional studies. Derived from the human KYSE-150 esophageal squamous cell carcinoma line, this polyclonal pool harbors targeted disruption of the KAT7 gene, generating a loss-of-function model that avoids the time and expense of single-cell cloning. The population is suitable for immediate use in assays that require averaged responses from heterogeneous knockout alleles.
KYSE-150 is a well-differentiated esophageal squamous cell carcinoma line that faithfully recapitulates molecular hallmarks of esophageal cancer, including aberrant cell cycle control and DNA replication dynamics. Its origin from a primary tumor makes it a physiologically relevant host for probing epigenetic mechanisms underlying esophageal carcinogenesis and for preclinical evaluation of therapeutic interventions.
KAT7 (lysine acetyltransferase 7, also known as HBO1) is the catalytic subunit of the HBO1 acetyltransferase complex, which also contains the scaffold proteins ING5, JADE1/2/3, and BRPF1. KAT7 specifically acetylates histone H3 at lysine 14 (H3K14ac) and histone H4 at lysines 5, 8, and 12 (H4K5ac, H4K8ac, H4K12ac) at replication origins. This acetylation is prerequisite for recruitment of the MCM2-7 helicase complex by the origin recognition complex (ORC), CDC6, and CDT1, thereby licensing DNA replication. KAT7 activity is directly regulated by Cyclin E/CDK2 and E2F transcription factors, tying it to the G1/S transition. Additionally, KAT7 acetylates p53, modulating its transcriptional activity, and participates in Wnt pathway-dependent chromatin regulation. Thus, KAT7 integrates replication licensing with cell cycle progression and transcriptional programs.
In esophageal squamous cell carcinoma, KAT7 dysregulation contributes to unchecked proliferation and genomic instability. The KYSE-150 knockout model enables detailed analysis of KAT7-dependent phenotypes in a cell type directly relevant to esophageal cancer, as well as to related malignancies such as hepatocellular carcinoma and gastric cancer. Disrupting KAT7 in these cells is expected to impair origin licensing, delay S-phase entry, and reduce histone acetylation, providing a platform for exploring the causal links between epigenetic deregulation and oncogenesis. Moreover, the model can be used to investigate the interplay between replication stress, DNA damage response, and chromatin modifications.
Researchers can use this polyclonal knockout population to monitor MCM2-7 chromatin loading by chromatin fractionation, assess global histone acetylation changes via western blotting (H3K14ac, H4K5ac, H4K8ac, H4K12ac), and perform cell cycle analysis by flow cytometry. EdU incorporation assays quantify DNA synthesis rates, while colony formation assays evaluate long-term proliferation. Co-immunoprecipitation of HBO1 complex components (e.g., ING5, JADE1, BRPF1) confirms complex integrity, and RT-qPCR measures expression of downstream factors like MCM2-7 subunits. The model is also suited for drug target validation, synthetic lethality screens, and study of epigenetic therapies. For additional technical information, please contact Ascent Research.
