The BCOR Knouckout SK-HEP-1 Polyclonal Cells constitute a CRISPR/Cas9-edited polyclonal knockout cell population in which the BCOR gene has been disrupted to generate a loss-of-function model. This product provides a heterogeneous pool of edited cells, enabling researchers to study BCOR-dependent functions without the confounding effects of clonal selection. The polyclonal format preserves genetic diversity and mitigates potential off-target artifacts, making it suitable for robust functional genomics studies.
The host cell line SK-HEP-1 is a human liver adenocarcinoma cell line originally isolated from ascitic fluid of a male patient. SK-HEP-1 cells display a unique dual phenotype with both epithelial and endothelial characteristics, rendering them a versatile model for hepatic adenocarcinoma and angiogenesis research. Their endothelial-like properties allow investigation of transdifferentiation and vascular mimicry in the tumor microenvironment.
BCOR encodes a transcriptional corepressor that functions as a critical component of Polycomb repressive complex 1.1 (PRC1.1) and mediates gene silencing by interacting with BCL6. Through BCL6 recruitment, BCOR assembles a repressive complex containing PCGF1, RING1B/RNF2, KDM2B, and histone deacetylases, leading to histone H2A ubiquitination and chromatin compaction. This complex directly represses key tumor suppressor genes including p53/TP53, BBC3/PUMA, PMAIP1/NOXA, and CDKN1A/p21, thereby regulating cell proliferation, apoptosis, and differentiation. BCOR activity intersects with Wnt and Notch signaling pathways, linking developmental cues to transcriptional programs.
In the context of SK-HEP-1 cells, BCOR knockout provides a physiologically relevant system to dissect the tumor suppressor roles often attributed to BCOR in hepatocellular carcinoma. The dual epithelial-endothelial nature of SK-HEP-1 enables examination of BCOR??s impact on both carcinomatous progression and vascular mimicry. Disruption of BCOR-mediated repression is expected to alter the expression of downstream effectors such as p53 and p21, potentially affecting cell cycle control, apoptosis, and migratory capacity. This model thus facilitates exploration of epigenetic silencing mechanisms in liver cancer and the interplay between transcriptional repression and tumor angiogenesis.
Researchers may employ this polyclonal knockout model for diverse applications including Western blotting and RT-qPCR validation of BCOR target gene expression, transcriptome profiling via RNA-seq, and co-immunoprecipitation to assess BCL6/BCOR complex integrity. Functional assays such as flow cytometry for apoptosis and cell cycle analysis, migration and invasion assays, and xenograft tumor growth studies are highly compatible. The system is also amenable to drug sensitivity screening, particularly against HDAC inhibitors, given BCOR??s involvement in histone deacetylation. For further details regarding this product, please contact Ascent Research.
