The BRPF3 Knockout HCT 116 Polyclonal Cells are a CRISPR/Cas9-edited human cell population engineered for targeted disruption of the BRPF3 gene within the HCT 116 colorectal carcinoma line. As a polyclonal knockout pool, this model circumvents clonal selection bias and provides a heterogeneous genetic background that more faithfully recapitulates the variability inherent in tumor cell populations. The ablation of BRPF3, achieved through CRISPR/Cas9-mediated genomic editing, creates a loss-of-function system to dissect the scaffold protein??s role in histone acetyltransferase (HAT) complex assembly and chromatin-directed transcriptional regulation. This product is supplied as a ready-to-use polyclonal knockout cell population, facilitating reproducible experiments in epigenetics and cancer biology without the need for single-cell cloning.
The host HCT 116 cell line is a well-characterized male-derived human colorectal carcinoma model exhibiting high microsatellite instability (MSI-H), a KRAS G13D driver mutation, and wild-type p53 status. These cells are highly proliferative, tumorigenic, and widely employed in colorectal cancer research due to their defined genetic landscape and responsiveness to extrinsic signals. The HCT 116 background is particularly relevant for studying the interplay between oncogenic KRAS/MAPK signaling, Wnt/??-catenin-driven transcription, and epigenetic regulation, as these pathways converge to govern proliferation, differentiation, and survival. The integration of a BRPF3 knockout into this context enables direct interrogation of chromatin modifier function within a disease-relevant, genetically tractable system.
BRPF3 functions as an essential scaffold within the MOZ (KAT6A)/MORF (KAT6B) histone acetyltransferase complexes, where it bridges the catalytic subunits with adapter proteins ING5 and EAF6, and serves as a reader of acetylated histone H3. Through these interactions, BRPF3 directs the acetylation of histone H3 at lysine 9 and lysine 14 (H3K9ac and H3K14ac), promoting open chromatin architecture and transcriptional activation of target gene programs. Upstream, BRPF3-mediated acetylation is regulated by Wnt/??-catenin signaling via TCF/LEF transcription factors, KRAS/MAPK pathway effectors, and cell cycle controls. Downstream, BRPF3-containing complexes critically regulate HOX gene clusters, cell cycle genes, and proliferation/differentiation determinants. Disruption of BRPF3 uncouples HAT activity from its chromatin-targeting apparatus, leading to altered histone acetylation landscapes and dysregulated gene expression.
Within the HCT 116 colorectal carcinoma environment, BRPF3 knockout disrupts the delicate balance of histone modification that sustains oncogenic transcription. The BRPF3-dependent acetyltransferase complexes act downstream of constitutively active Wnt/??-catenin and mutant KRAS signaling, making them vulnerable nodes in the epigenetic maintenance of the malignant state. Loss of BRPF3 is expected to reduce local H3K9/K14 acetylation at promoters of HOX and cell cycle regulators, thereby impairing the proliferative capacity and differentiation status characteristic of HCT 116 cells. This model thus illuminates how scaffolding proteins within HAT complexes couple upstream oncogenic inputs to chromatin outputs and offers a platform to assess synthetic lethal interactions or sensitivity to targeted agents that exploit epigenetic vulnerabilities in KRAS-mutant colorectal cancer.
This BRPF3 polyclonal knockout cell pool supports a wide array of research applications in chromatin biology, cancer epigenetics, and functional genomics. Typical assays include Western blotting for BRPF3 and acetylated H3 marks (H3K9ac, H3K14ac), RT-qPCR analysis of HOX and cell cycle gene expression, RNA-sequencing to map transcriptional changes, ChIP-qPCR to probe locus-specific histone modifications, co-immunoprecipitation to assess residual complex integrity, and cell-based assays monitoring proliferation, apoptosis, and drug sensitivity. These cells are particularly suited for mechanistic studies linking chromatin regulation to colorectal cancer pathogenesis and for drug target identification in epigenetically driven malignancies. For further details or customized support, please contact Ascent Research.
