The BRD8 Knockout KYSE-150 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population in which the BRD8 gene has been disrupted in the human KYSE-150 esophageal squamous cell carcinoma (ESCC) line. This engineered cell pool provides a loss-of-function model for investigating BRD8-dependent mechanisms, offering a heterogeneous population reflecting diverse editing outcomes suitable for pooled functional analyses while reducing clonal bias.
The KYSE-150 cell line, derived from a poorly differentiated ESCC, is widely used as an in vitro model for esophageal cancer research. It retains key tumorigenic features, including aberrant growth and signaling pathways commonly altered in ESCC. The combination of this clinically relevant background with targeted BRD8 disruption makes the polyclonal knockout population especially valuable for studying chromatin dysregulation linked to esophageal tumorigenesis.
BRD8 encodes a bromodomain-containing core subunit of the NuA4/TIP60 histone acetyltransferase complex, which acetylates histone H4 to promote chromatin relaxation and transcriptional activation. BRD8 interacts with TRRAP, EPC1, ING3, and the catalytic TIP60 subunit. Upstream, DNA damage-activated ATM/ATR kinases signal to the NuA4 complex, influencing downstream effectors including p53, p21, and acetylated H4. BRD8 disruption destabilizes complex integrity, reducing H4 acetylation, impairing p53-driven transcription, and compromising DNA double-strand break repair, thereby linking chromatin modification to cell cycle control and genomic stability.
In KYSE-150 cells, BRD8 knockout attenuates NuA4-mediated chromatin remodeling, potentially altering oncogenic gene expression and DNA damage responses characteristic of ESCC. This model enables investigation of BRD8’s role in tumor maintenance and may reveal sensitivities to genotoxic stress or bromodomain-targeted inhibitors. The polyclonal nature allows assessment of population-level effects, providing a robust platform for mechanistic and therapeutic studies in esophageal cancer.
Applications include functional dissection of the NuA4/TIP60 complex, chromatin remodeling research, and DNA damage response studies. Typical assays involve Western blotting for acetylated histones, RT-qPCR for p21, ??-H2AX immunofluorescence, ChIP-qPCR for H4 acetylation, and flow cytometry for cell cycle analysis. The cells also support drug screening and epigenetic investigations. For further information, contact Ascent Research.
