KAT6A Knockout HT29 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population derived from the HT29 colorectal adenocarcinoma cell line, designed for loss-of-function studies of the lysine acetyltransferase 6A (KAT6A) gene. The polyclonal pool contains heterogeneous gene disruptions at the KAT6A locus, enabling robust assessment of KAT6A-dependent phenotypes without clonal selection bias and providing a versatile tool for functional genomics in cancer research.
HT29 is a human colorectal adenocarcinoma cell line originating from a primary tumor, exhibiting epithelial morphology, and widely employed as a model in cancer research, particularly for intestinal epithelial barrier studies and colorectal tumorigenesis. Its well-characterized growth characteristics and genetic background make it a suitable host for investigating epigenetic mechanisms that drive colorectal cancer progression and drug responses.
KAT6A is a histone acetyltransferase that specifically acetylates histone H3 at lysine 9 and lysine 14 (H3K9ac/H3K14ac), promoting chromatin relaxation and transcriptional activation. It forms a functional complex with the scaffold proteins BRPF1 or BRPF2, along with ING5 and EAF6, which directs its catalytic activity. Upstream regulators include RUNX1, CBF??, PU.1, NOTCH1, and ??-catenin, linking KAT6A to diverse developmental and oncogenic pathways. Upon activation, KAT6A acetylates histones at gene promoters of key downstream targets such as p53, HOXA9, MYC, CD34, and CDKN1A, thereby modulating their expression. Direct interaction with p53 and RUNX1 further contributes to p53 acetylation and transcriptional coactivation, influencing cell cycle arrest, apoptosis, and differentiation. Through these interactions, KAT6A integrates signals from the p53, Wnt, and Notch pathways, making it a nexus in hematopoietic and intestinal epithelial cell fate decisions.
In the HT29 colorectal cancer model, disruption of KAT6A impairs histone acetylation and p53 acetylation, leading to altered transcriptional programs that govern cell proliferation, apoptosis, and differentiation. Given the frequent dysregulation of Wnt/??-catenin and p53 signaling in colorectal cancer, this knockout model provides a tractable system to dissect epigenetic modulation of tumor suppressor and oncogene networks. The polyclonal format captures a range of loss-of-function effects, reflecting the heterogeneity observed in tumor cell populations and enabling more robust phenotypic analysis without reliance on single clones.
These KAT6A knockout HT29 cells support a wide range of experimental applications, including western blotting and ChIP-qPCR to monitor histone acetylation dynamics, RT-qPCR and RNA-seq for transcriptome-wide analysis of KAT6A targets, and flow cytometry or colony formation assays to assess cell cycle and apoptotic responses. The model is well-suited for investigating epigenetic mechanisms downstream of Wnt/??-catenin and p53, functional analysis of p53 acetylation, and screening of small-molecule acetyltransferase inhibitors. Migration and invasion assays can further evaluate KAT6A??s role in colorectal cancer metastasis. For additional information or custom applications, please contact Ascent Research.
