The HMG20B knockout SK-HEP-1 polyclonal cells are a CRISPR/Cas9-edited loss-of-function model in which the HMG20B gene has been disrupted in the human hepatic adenocarcinoma SK-HEP-1 cell line. Supplied as a polyclonal knockout cell population, this product provides a heterogeneous collection of HMG20B-disrupted cells for studying the gene??s role in transcriptional repression and tumor biology without requiring single-cell cloning.
SK-HEP-1 is a hepatic adenocarcinoma cell line established from the ascites of a liver cancer patient. It displays mesenchymal and invasive characteristics and is tumorigenic in immunodeficient mice, making it a relevant model for liver cancer metastasis, angiogenesis, and drug resistance. Its background supports investigations into how chromatin modifiers influence hepatic tumor progression.
HMG20B is a core subunit of the BRAF35/HDAC repressor complex, recruited by REST to RE1 sites in neuronal gene promoters. It facilitates transcriptional silencing via HDAC1/2-mediated deacetylation and KDM1A-mediated demethylation, directly interacting with REST, RCOR1, and PHF21A. Beyond neuronal genes, HMG20B is regulated by E2F and ATM/ATR kinases and influences cell cycle genes (CCNB1, CDK1) and DNA repair factors (BRCA1, RAD51), positioning it at the intersection of epigenetic silencing, cell division, and genome integrity.
In the SK-HEP-1 hepatic adenocarcinoma context, HMG20B knockout is predicted to derepress REST target genes, potentially reducing the mesenchymal invasive phenotype and altering DNA damage responses. This disruption may affect proliferation, differentiation, and sensitivity to HDAC inhibitors, offering a tractable system to connect chromatin-based gene regulation with liver cancer aggressiveness.
This knockout model supports applications such as REST complex functional dissection, epigenetic drug target validation, CRISPR-based synthetic lethality screens, and analysis of neuronal gene derepression in non-neural tumors. Representative experimental approaches include Western blotting, RT-qPCR, ChIP-qPCR, transwell migration/invasion assays, RNA-seq profiling, and HDAC inhibitor sensitivity testing. For further details or custom configurations, please contact Ascent Research.
