The BRD8 Knockout HGC-27 Polyclonal Cells comprise a CRISPR/Cas9-mediated polyclonal knockout cell population derived from HGC-27 gastric carcinoma cells, featuring targeted disruption of the BRD8 gene. This heterogeneous pool preserves population diversity while abrogating BRD8 function, providing a robust loss-of-function model in a metastatic gastric adenocarcinoma background. The product is supplied as live cells validated for BRD8 deficiency, ready for expansion and downstream functional assays.
HGC-27 is a human gastric carcinoma epithelial cell line originating from a lymph node metastasis of a poorly differentiated gastric adenocarcinoma. It serves as a well-characterized in vitro model for metastatic gastric cancer, displaying aggressive growth and epithelial morphology. HGC-27 cells are widely utilized in oncology research to investigate mechanisms of metastasis, drug resistance, and tumor progression, making them an ideal host for studying gene function in advanced gastric cancer.
BRD8 is a scaffolding subunit of the NuA4/TIP60 histone acetyltransferase complex, which acetylates histones H4 and H2A to relax chromatin and activate transcription. It interacts with EP400, TRRAP, KAT5/TIP60, RUVBL1, RUVBL2, and ACTL6A to assemble the complex. Upstream, BRD8 is regulated by TP53, MYC, E2F factors, and DNA damage signaling via ATM/ATR. Downstream, BRD8-dependent acetylation promotes expression of CCND1, CDKN1A, and MYC targets. Thus, BRD8 integrates oncogenic and tumor-suppressive signals to coordinate chromatin remodeling, transcriptional regulation, and cell cycle control.
In HGC-27 gastric cancer cells, BRD8 knockout disrupts NuA4/TIP60 function, reducing histone acetylation and impairing transcriptional programs that drive aggressiveness. This perturbation compromises DNA repair and alters proliferation, providing a tool to study epigenetic mechanisms of metastasis. Given BRD8’s roles in colorectal, hepatocellular, and glioblastoma cancers, the model is relevant across multiple malignancies. Thus, it enables dissection of BRD8-dependent chromatin regulation in tumor biology.
This polyclonal knockout is suited for diverse assays: western blotting for acetylated histones, RT-qPCR for CCND1 and MYC, ChIP-qPCR for H4ac at promoters, MTS proliferation, colony formation, ??-H2AX foci for DNA damage, cell cycle analysis by flow cytometry, and RNA-seq. These enable comprehensive studies of BRD8 in epigenetic regulation and support drug target validation and biomarker discovery. For more information, contact Ascent Research.
