The HMG20B Knockout HT29 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal cell population derived from the HT29 colorectal adenocarcinoma line, designed for targeted disruption of the HMG20B gene. This pooled knockout model avoids clonal selection artifacts and reflects population-level gene disruption, enabling robust functional studies of HMG20B in chromatin remodeling and transcriptional repression.
The HT29 parental cell line is an epithelial model originating from a colorectal adenocarcinoma of a 44-year-old female. HT29 cells are capable of enterocyte-like differentiation, producing mucin and forming intestinal barrier-like structures under specific conditions. This characteristic makes the HMG20B knockout in HT29 particularly relevant for examining the epigenetic control of colorectal tumorigenesis, differentiation, and metastasis-related pathways.
HMG20B is a core subunit of the BHC/CoREST repressor complex, which includes CoREST (RCOR1), HDAC1, HDAC2, and LSD1 (KDM1A). Recruited by the transcription factor REST to neuronal gene promoters, HMG20B facilitates histone H3 and H4 deacetylation and H3K4 demethylation, leading to silencing of REST target genes such as BDNF and SYN1. Knockout of HMG20B disrupts this repressive machinery, permitting derepression of these targets and enabling functional dissection of REST-dependent gene silencing pathways.
Within the HT29 colorectal carcinoma system, HMG20B knockout provides a physiologically relevant tool to study the role of CoREST-mediated chromatin remodeling in cancer cell biology. Disruption of HMG20B is expected to alter histone acetylation patterns, reactivate silenced target genes, and modulate cellular phenotypes including proliferation, migration, and drug responses. This model thus bridges epigenetics and colorectal cancer research, facilitating studies on how REST/CoREST dysfunction contributes to malignant progression.
This polyclonal knockout pool is suitable for diverse assays, including Western blotting for HMG20B, RT-qPCR for REST target transcripts, ChIP-qPCR for histone modifications, and ATAC-seq for chromatin accessibility. Functional studies such as MTT proliferation, migration/invasion assays, and immunofluorescence for the CoREST complex are readily performed. Additionally, the cells serve as an epigenetically relevant system for screening inhibitors of HDAC1/2 or LSD1. For further technical details, assay guidance, or customization requests, please contact Ascent Research.
