The BAZ2B Knockout SK-HEP-1 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population designed to disrupt BAZ2B gene function in the human SK-HEP-1 hepatic adenocarcinoma cell line. This polyclonal product provides a loss-of-function model without single-cell cloning, preserving genetic heterogeneity while achieving targeted gene disruption. It is ideal for population-level analyses, including biochemical and phenotypic assays where a mixed knockout background is advantageous, such as drug sensitivity screens or functional genomics studies.
SK-HEP-1, derived from the ascites of a patient with liver adenocarcinoma, serves as a widely used model for hepatocellular carcinoma (HCC) and displays mixed epithelial and endothelial features. This unique phenotype makes it valuable for investigating tumor cell plasticity, angiogenic signaling, and the molecular basis of hepatic cancer. The cell line provides a robust platform for studying epigenetic dysregulation and chromatin remodeling in HCC.
BAZ2B is a core component of the nucleolar remodeling complex (NoRC), where it forms complexes with SMARCA5 (SNF2H), HDAC1, and DNMT1 to silence ribosomal DNA (rDNA) transcription. Through histone deacetylation and DNA methylation, this complex establishes a repressive heterochromatin state at rDNA loci. Upstream, BAZ2B expression is transcriptionally regulated by MYC, linking oncogenic growth signals to ribosomal biogenesis. Knockout of BAZ2B disrupts NoRC integrity, deepressing pre-rRNA synthesis and ribosomal protein gene expression, and leading to enhanced nucleolar activity and altered cell proliferation.
In the SK-HEP-1 hepatic adenocarcinoma context, BAZ2B knockout enables detailed investigation of NoRC-dependent ribosomal regulation in liver cancer. Loss of BAZ2B is predicted to derepress rDNA, modify nucleolar morphology, and shift the balance between proliferation and apoptosis. This model facilitates exploration of epigenetic vulnerabilities in HCC and the therapeutic potential of targeting ribosomal silencing, while the mixed epithelial/endothelial background allows assessment of BAZ2B’s role in tumor cell heterogeneity.
Researchers can apply this knockout model in chromatin immunoprecipitation (ChIP)-qPCR to assess histone modifications at rDNA, RT-qPCR for rRNA expression, and western blotting to evaluate NoRC complex components. Immunofluorescence for nucleolar integrity, proliferation assays, and RNA-seq analyses further characterize BAZ2B loss. These cells also support studies of MYC-NoRC crosstalk in hepatic cancer. For further information, please contact Ascent Research.
