The CBX3 Knockout SK-HEP-1 Polyclonal Cells consist of a CRISPR/Cas9-edited heterogeneous population of the SK-HEP-1 hepatic endothelial-like cell line, engineered to disrupt the CBX3 gene. This polyclonal pool contains diverse genomic modifications that collectively abrogate CBX3 expression, providing a loss-of-function model for investigating the chromobox protein homolog 3. The format circumvents clonal selection bottlenecks and captures a broad spectrum of knockout variants, making these cells well-suited for functional genomics studies, epigenetic research, and drug discovery applications.
The SK-HEP-1 host line, isolated from ascitic fluid of a 52-year-old male with hepatic adenocarcinoma of unknown primary origin, displays an endothelial phenotype. Expressing endothelial differentiation markers, it is widely used as a liver sinusoidal endothelial cell model. The line??s unique tumor-endothelial background makes it a powerful tool for studying tumor angiogenesis, vascular biology, and microenvironment crosstalk, providing a context for cancer metastasis and endothelial-tumor interactions.
CBX3 acts as a reader of H3K9me3, mediating heterochromatin formation and gene silencing through interactions with HP1??/CBX5, HP1??/CBX1, SUV39H1, and Lamin B receptor, tethering chromatin to the nuclear lamina. In addition, CBX3 contributes to transcriptional elongation and cell cycle control. It is regulated upstream by p53 and E2F1 transcription factors, and it transcriptionally modulates downstream effectors such as the cell cycle inhibitor p21/CDKN1A, cyclin D1, and E-cadherin, linking epigenetic silencing to proliferative and invasive pathways.
In the SK-HEP-1 endothelial context, CBX3 knockout enables investigation of heterochromatin dynamics in angiogenesis and endothelial function. With CBX3 involved in p53/E2F1 pathways, this model is valuable for epigenetic studies of hepatocellular carcinoma and cancers where endothelial behavior drives progression. Researchers can probe whether CBX3 loss affects angiogenic factor expression, junctional integrity, and endothelial cell cycle, illuminating how chromatin readers impact the endothelial-tumor interface.
Applications include ChIP-qPCR to measure H3K9me3 enrichment, Western blotting and RT-qPCR for downstream target analysis, and immunofluorescence for heterochromatin imaging. Flow cytometry-based cell cycle analysis, proliferation, migration, and invasion assays can define functional phenotypes. The polyclonal population supports pooled screening and population-level epigenetic profiling. For further technical details, please contact Ascent Research.
