KAT7 Knockout HCT 116 Polyclonal Cells represent a CRISPR/Cas9-edited polyclonal knockout cell population designed to disrupt the KAT7 gene in the human HCT 116 colorectal carcinoma cell line. This polyclonal mixture contains a heterogeneous collection of edited cells, providing a robust loss-of-function model for studying KAT7-dependent processes without the need for single-cell clonal isolation.
The HCT 116 cell line is a well-characterized human epithelial colorectal carcinoma model with a stable genome, widely used in cancer research. These cells harbor activating mutations in KRAS and ??-catenin, and exhibit intact DNA damage and cell cycle checkpoints, making them an ideal platform for dissecting epigenetic regulation of proliferation and replication dynamics.
KAT7 (also known as MYST2 or HBO1) encodes a histone acetyltransferase that specifically acetylates histone H3 at lysine 14 (H3K14) and histone H4 at lysines 5, 8, and 12 (H4K5/K8/K12). It functions as the catalytic subunit of the MYST2 acetyltransferase complex, which includes adaptor proteins ING4, ING5, JADE1/2/3, EAF6, and MEAF6. KAT7 activity is regulated by CDK2/cyclin E-mediated phosphorylation in response to growth factor signaling. Downstream, KAT7-mediated acetylation facilitates chromatin relaxation at replication origins, enabling the assembly of pre-replicative complexes containing ORC, CDC6, and the MCM2-7 helicase, thereby licensing origins for DNA replication.
In HCT 116 cells, disruption of KAT7 leads to impaired origin firing, delayed S-phase progression, and altered transcriptional programs due to reduced histone acetylation at critical genomic loci. Given the reliance of colorectal cancer cells on robust proliferation and replication licensing, loss of KAT7 function can compromise cell growth and survival, highlighting its potential as a therapeutic vulnerability. The polyclonal knockout population allows researchers to rapidly assess the functional consequences of KAT7 ablation in a relevant cancer model, while avoiding clonal artifacts.
Researchers can employ this model in a variety of assays, including Western blotting and ChIP-qPCR to assess histone acetylation changes, flow cytometry and EdU incorporation to monitor cell cycle dynamics, colony formation assays to evaluate long-term proliferative capacity, and RNA-seq to profile transcriptome-wide effects. Co-immunoprecipitation experiments can further elucidate interaction networks with MYST2 complex components. These applications make the KAT7 Knockout HCT 116 Polyclonal Cells a valuable tool for cancer epigenetics, DNA replication studies, and drug target validation. For additional product information and technical support, please contact Ascent Research.
