The HP1BP3 Knockout SK-HEP-1 Polyclonal Cells represent a pooled population of SK-HEP-1 cells subjected to CRISPR/Cas9-mediated disruption of the HP1BP3 gene, enabling loss-of-function analysis of HP1BP3 in a heterogeneous cell pool. This polyclonal knockout product provides a robust cellular model for investigating HP1BP3-dependent heterochromatin organization and gene silencing without the clonal selection artifacts often associated with single-cell-derived lines. The targeted gene disruption abrogates HP1BP3 protein expression, offering a physiologically relevant system for functional genomics and drug target validation studies.
Derived from the ascites of a patient with liver adenocarcinoma, the SK-HEP-1 host cell line is a widely used model for hepatocellular carcinoma (HCC) and metastasis research. These cells display an endothelial-like phenotype and have been instrumental in dissecting molecular mechanisms underlying HCC tumorigenesis, invasion, and therapeutic resistance. The SK-HEP-1 background provides a clinically pertinent context for examining the contributions of epigenetic regulators like HP1BP3 to liver cancer biology and for evaluating novel therapeutic strategies targeting chromatin-associated proteins.
HP1BP3 encodes a linker histone-like chromatin-binding protein that functions as a critical architectural component of heterochromatin. It directly interacts with the chromodomain proteins CBX1 (HP1??), CBX3 (HP1??), and CBX5 (HP1??), as well as with the heterochromatin mark histone H3K9me3, to facilitate chromatin compaction and gene repression. HP1BP3 also associates with the lamin B receptor (LBR) and the histone methyltransferase SETDB1, reinforcing pericentromeric heterochromatin integrity. Its activity is modulated by upstream cell cycle kinases such as CDK1, DNA damage sensors including ATM and ATR, and transcription factors like E2F. Consequently, HP1BP3 serves as a nexus integrating signals from cell cycle progression, DNA damage response, and global gene expression programs through its regulation of chromatin accessibility.
Disrupting HP1BP3 in the SK-HEP-1 liver adenocarcinoma model is anticipated to perturb heterochromatin maintenance, potentially resulting in chromatin decondensation, aberrant gene expression profiles, and altered cellular phenotypes relevant to cancer. Given the role of HP1BP3 in regulating proliferation-associated and DNA repair genes, this knockout population enables exploration of how epigenetic dysregulation contributes to unchecked growth, genomic instability, and metastatic potential in HCC. Researchers can employ this model to dissect the dependency of liver cancer cells on HP1BP3-mediated silencing for survival and to investigate synthetic lethal interactions with other chromatin modifiers or DNA damage pathway components.
This product is suited for a broad range of experimental workflows, including chromatin immunoprecipitation followed by quantitative PCR (ChIP-qPCR) to assess histone modification changes, assay for transposase-accessible chromatin with high-throughput sequencing (ATAC-seq) for chromatin accessibility profiling, and immunofluorescence to visualize heterochromatin architecture. Functional assays such as MTT proliferation and Transwell migration assays can quantify the impact of HP1BP3 loss on cancer cell behavior. Combining these with RT-qPCR and Western blotting validates downstream targets. For inquiries regarding technical specifications or bulk orders, please contact Ascent Research.
