KAT6B Knockout HT29 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population derived from the HT29 human colorectal adenocarcinoma cell line. This product comprises a heterogeneous pool of cells with targeted disruption of the KAT6B gene, achieved through CRISPR/Cas9-mediated gene editing. The polyclonal format ensures diverse knockout alleles, enabling robust functional analysis without clonal selection bias and serving as a valuable tool for studying epigenetic mechanisms in a malignant epithelial background.
The HT29 cell line, isolated from a female patient with colorectal adenocarcinoma, displays epithelial morphology and a proliferative, partially differentiated phenotype. HT29 cells are characterized by an APC mutation that constitutively activates WNT/??-catenin signaling, making them a widely used model for colon cancer research. Their well-established growth characteristics and genetic tractability render them an ideal host for CRISPR-mediated gene editing to investigate oncogenic transcriptional regulation and therapeutic vulnerabilities.
KAT6B encodes a histone acetyltransferase of the MYST family that specifically acetylates histone H3 at lysine 23 (H3K23ac) and functions as a transcriptional coactivator within the tetrameric BRPF1-ING5-EAF6 complex. This complex is recruited to chromatin by transcription factors including RUNX1, RUNX2, and CDX2, and its activity is stimulated by upstream WNT/??-catenin signaling. KAT6B-mediated H3K23 acetylation promotes the expression of key downstream targets such as HOXA cluster genes, CCND1, MYC, and CDKN1A. Additionally, KAT6B interacts with ING4 and p53 through ING5, bridging histone modification and tumor suppression. Knockout of KAT6B eliminates its acetyltransferase activity, leading to reduced H3K23ac at target gene promoters and disruption of the coactivator complex, ultimately impairing WNT-driven proliferative and developmental transcriptional programs.
In HT29 cells with constitutive WNT activation, ablation of KAT6B likely attenuates oncogenic transcription, shifting the balance from proliferation toward differentiation and apoptosis. Reduced H3K23ac at promoters of CCND1 and HOXA9 exemplifies the epigenetic dependence of colon cancer cells on KAT6B for sustained growth. This knockout model enables precise investigation of KAT6B??s role in colorectal tumorigenesis, including its impact on cell cycle control, survival, and migration, and provides a platform for evaluating chromatin-based therapeutic interventions.
The KAT6B Knockout HT29 Polyclonal Cells are suitable for a broad array of research applications, including functional characterization of KAT6B in colorectal cancer, mechanistic dissection of histone acetylation pathways, and validation of small-molecule HAT inhibitors. Representative assays include Western blotting for KAT6B and H3K23ac, RT-qPCR for HOXA9 and CCND1, ChIP-qPCR for promoter H3K23ac, MTT and annexin V assays for proliferation and apoptosis, Boyden chamber migration assays, RNA-seq transcriptomics, and colony formation studies. For further information, please contact Ascent Research.
