BCOR Knockout HT29 Polyclonal Cells consist of human colorectal adenocarcinoma HT29 cells engineered via CRISPR/Cas9 to disrupt the BCOR gene. The polyclonal population contains heterogeneous editing outcomes, offering a loss-of-function model for studying BCOR-dependent processes. Ablation of BCOR protein eliminates its corepressor function, permitting investigation of transcriptional derepression. This product is suitable for functional genomics assays and phenotypic screens in a colorectal cancer epithelial background.
The HT29 cell line originates from a primary colorectal adenocarcinoma of a 44-year-old female. These epithelial cells are widely used as a model of human intestinal epithelium and retain the ability to undergo differentiation under appropriate conditions, making them valuable for colonocyte maturation studies. HT29 cells harbor mutations in APC, TP53, and KRAS typical of colorectal cancer, contributing to tumorigenicity. Their well-characterized genetic background and responsiveness to stimuli facilitate mechanistic studies of colorectal carcinogenesis.
BCOR encodes the BCL6 corepressor, a component of non-canonical Polycomb repressive complex 1 (PRC1.1). Within PRC1.1, BCOR interacts with BCL6 and PCGF1, recruiting RING1B and RYBP to catalyze monoubiquitination of histone H2A at lysine 119 (H2AK119ub1). This modification silences target genes such as CDKN1A, CDKN2A, and HOX genes. BCOR activity is modulated by retinoic acid signaling and BCL6. Knockout of BCOR disrupts PRC1.1 function, reducing H2AK119ub1 and relieving repression of genes that promote cell cycle arrest and apoptosis. This model enables dissection of BCOR, Polycomb proteins, and BCL6-mediated repression interplay.
In colorectal cancer, BCOR may function as a context-dependent tumor suppressor; its loss is linked to aggressive phenotypes in some malignancies. While BCOR mutations are uncommon in colorectal cancer, epigenetic silencing might contribute to tumor progression. The HT29 polyclonal knockout system allows assessment of how BCOR inactivation affects proliferation, differentiation, apoptosis, and drug sensitivity. Comparing knockout and parental cells reveals BCOR-dependent pathways and whether its loss promotes or suppresses oncogenic traits. This system also aids study of Polycomb-mediated gene silencing in malignant phenotypes.
BCOR Knockout HT29 Polyclonal Cells are suitable for a wide range of experiments. Western blotting and RT-qPCR verify BCOR protein loss and derepression of CDKN1A and CDKN2A. ChIP-qPCR quantifies H2AK119ub1 enrichment at Polycomb target genes. Cell proliferation, colony formation, and flow cytometric cell cycle analysis reveal growth phenotypes, while transcriptome profiling by RNA-seq identifies global expression changes. Additionally, apoptosis assays, migration and invasion studies, and drug sensitivity screens assess functional consequences of BCOR loss. For further details, contact Ascent Research.
