KAT7 Knockout KYSE-30 Polyclonal Cells are a ready-to-use CRISPR/Cas9-edited polyclonal knockout cell population designed for studying the loss of function of the KAT7 gene. This product provides a heterogeneous pool of cells bearing targeted disruptions in KAT7, generated by CRISPR/Cas9-mediated gene editing in the KYSE-30 esophageal squamous cell carcinoma line. As a polyclonal population, it reflects diverse editing events and is suitable for experiments where a mixed knockout background is advantageous, such as pooled functional screens or bulk phenotypic analyses, without the need for single-cell cloning.
The host cell line, KYSE-30, is a well-established model of esophageal squamous cell carcinoma derived from a 64-year-old male patient with a well-differentiated invasive esophageal carcinoma. KYSE-30 cells maintain features of squamous differentiation and are widely employed in cancer research to investigate mechanisms of esophageal carcinogenesis, metastasis, and therapeutic resistance. Their relevance to esophageal cancer biology makes them an ideal background for interrogating epigenetic regulators implicated in this malignancy.
KAT7 encodes a histone acetyltransferase that specifically acetylates histone H4 at lysine residues K5, K8, and K12, modifications associated with open chromatin and active transcription. KAT7 functions as the catalytic subunit in complexes containing BRPF1, ING5, EAF6, and JADE1. Its activity is regulated by BRPF1 and ING5, and also by CDK2-mediated phosphorylation. Downstream, acetylation of histone H4 by KAT7 promotes chromatin relaxation and expression of proliferation-associated genes such as MYC and CDK1. Through these interactions, KAT7 links histone modification to cell cycle progression and DNA replication, with additional ties to Wnt signaling.
In esophageal squamous cell carcinoma, aberrant KAT7 activity drives oncogenic transcriptional programs sustaining tumor growth. Disruption of KAT7 in KYSE-30 cells provides a loss-of-function model to dissect chromatin dysregulation in this cancer. This system enables researchers to explore how loss of KAT7 acetylation impacts H4 modification dynamics, downstream gene expression, and proliferation, clonogenicity, and migration. It is valuable for identifying epigenetic vulnerabilities and validating KAT7 as a therapeutic target.
This KAT7 knockout polyclonal cell population is suited for applications including characterization of histone acetyltransferase function in cancer epigenetics, screening of small-molecule KAT7 inhibitors, and phenotypic analyses via Western blotting for histone H4 acetylation, RT-qPCR for MYC and CDK1 expression, cell viability assays, colony formation assays, migration assays, and ChIP-qPCR for H4K8ac. For further information, please contact Ascent Research.
