The KAT7 Knockout UM-UC-3 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population generated from the UM-UC-3 human bladder cancer line. This product provides targeted disruption of the KAT7 gene, which encodes a histone acetyltransferase responsible for acetylating histone H4 at K5, K8, and K12 and histone H3 at K14. The polyclonal format yields a heterogeneous pool of knockout cells, offering a robust loss-of-function system for studying KAT7-mediated epigenetic regulation and its role in tumor biology.
The parental UM-UC-3 cell line was established from a male patient with transitional cell carcinoma of the bladder and serves as an established model of invasive urothelial carcinoma. These adherent cells display epithelial morphology and retain key molecular features characteristic of advanced bladder cancer, making them valuable for investigating mechanisms of invasion, metastasis, and drug response within the urothelial carcinoma context.
KAT7 functions as a critical histone acetyltransferase that facilitates open chromatin by acetylating histones H4 and H3, thereby promoting transcriptional activation and DNA replication licensing. It forms multiprotein complexes with ING4/ING5 tumor suppressors, JADE1/2/3, and EAF6, and directly interacts with origin recognition complex subunits including ORC1 and CDT1. This positions KAT7 at the interface of histone modification and replication initiation, with upstream regulation by cell cycle kinases and downstream integration with p53 signaling. Disruption of KAT7 activity impairs histone acetylation, leading to compromised DNA replication licensing and widespread transcriptional changes that may alter tumorigenic behavior.
Within the invasive UM-UC-3 bladder cancer model, KAT7 knockout disrupts the epigenetic machinery that sustains malignant phenotypes. The loss of H4 and H3 acetylation can affect expression of genes controlling proliferation, apoptosis, and metastasis, thus enabling researchers to dissect how chromatin-level regulation contributes to urothelial carcinoma progression. This model is particularly suited for studying the interplay between KAT7-dependent acetylation and the p53 pathway, and for identifying vulnerabilities specific to bladder cancer cells.
These polyclonal knockout cells are amenable to diverse experimental approaches. Histone acetylation assays, ChIP, and western blotting for site-specific histone modifications directly probe epigenetic changes, while proliferation, cell cycle, and colony formation assays quantify functional consequences. Transcriptomic profiling via RNA-seq and replication focus analysis by immunofluorescence capture global effects on gene expression and DNA replication. For inquiries regarding this product or customization options, please contact Ascent Research.
