The BAZ2B Knockout HT29 Polyclonal Cells constitute a CRISPR/Cas9-edited polyclonal knockout cell population derived from HT29 human colorectal adenocarcinoma cells. This loss-of-function model targets BAZ2B, a gene encoding a bromodomain-containing chromatin remodeler. By disrupting BAZ2B expression in a heterogeneous cell pool, researchers can investigate its biological roles without clonal selection artifacts, maintaining the genetic diversity of the original tumor line.
Derived from a primary colorectal adenocarcinoma of a 44-year-old female, HT29 cells are polyploid and exhibit adherent epithelial morphology. While transformed, they retain the capacity for enterocytic differentiation under defined conditions, making them a versatile platform for intestinal epithelial and colorectal cancer studies. This host cell line is extensively characterized for drug response, signaling pathway analysis, and oncogenic phenotype investigation, offering a well-suited model to interrogate the tumor-related functions of BAZ2B.
BAZ2B is a core component of the NoRC and B-WICH nucleolar remodeling complexes, where it represses rRNA transcription by recognizing acetylated histone H3 through its bromodomain and recruiting histone deacetylases to rDNA repeats. It physically associates with SMARCA5, BAZ2A, BAZ1B, MYO1C, and ACTB to alter chromatin architecture at ribosomal gene loci. Activity is regulated by MYC signaling, histone H3 acetylation, and nucleolar stress signals, culminating in control of 45S pre-rRNA synthesis and ribosome biogenesis.
In the context of HT29 colorectal cancer, BAZ2B-mediated silencing of rDNA may counteract oncogene-driven ribosome overproduction, positioning it as a potential tumor suppressor. Knockout of BAZ2B in this model permits analysis of how loss of this epigenetic regulator affects nucleolar structure, stress pathways, and transformed cell growth. The model helps elucidate the interplay between chromatin silencing, nucleolar function, and malignant proliferation in a disease-relevant cellular environment.
This polyclonal knockout population is amenable to diverse assays, including western blotting for BAZ2B and nucleolar markers, RT-qPCR of 45S pre-rRNA, and ChIP-qPCR for H3K9ac at rDNA. It also supports immunofluorescence analysis of nucleolar proteins like nucleolin, nucleolar stress assays monitoring NPM1 translocation, and functional assessments such as cell viability and colony formation. These tools facilitate rigorous investigation of BAZ2B in epigenetic gene regulation and cancer biology. For further details, please contact Ascent Research.
