The JADE2 Knockout SK-HEP-1 Polyclonal Cells are a genetically engineered cell population derived from the SK-HEP-1 human liver adenocarcinoma line through CRISPR/Cas9-mediated disruption of the JADE2 gene. This polyclonal knockout product consists of a heterogeneous pool of cells harboring diverse loss-of-function mutations, providing a robust model for studying JADE2-dependent epigenetic and cell cycle regulation. By ablating JADE2 function, this system enables investigation of its scaffolding role in the HBO1 histone acetyltransferase complex, which is critical for chromatin remodeling and transcriptional control of S-phase progression.
The SK-HEP-1 host cell line was originally isolated from the ascites of a patient with liver adenocarcinoma and exhibits an adherent, epithelial-like morphology. As a widely adopted hepatocellular carcinoma model, SK-HEP-1 cells retain key features of malignant hepatocytes, including dysregulated proliferative signaling and altered gene expression profiles. This cellular background is particularly suited for exploring the molecular mechanisms driving liver cancer pathogenesis and for evaluating the contribution of epigenetic modifiers such as JADE2 to oncogenic phenotypes.
JADE2 functions as a scaffold protein within the HBO1 acetyltransferase complex, directing the specific acetylation of histone H4 at lysine residues K5, K8, and K12. This post-translational modification relaxes chromatin structure and facilitates the transcriptional activation of genes essential for DNA replication and cell cycle progression. JADE2 interacts directly with the catalytic subunit KAT7 (HBO1) and with regulatory cofactors including ING4, ING5, MEAF6, and PHF15. Upstream, JADE2 is modulated by E2F transcription factors and growth factor signaling pathways, while downstream it promotes expression of E2F target genes and licensing of DNA replication origins. Thus, depletion of JADE2 disrupts H4 acetylation dynamics, impairing S-phase entry and cell proliferation.
In the context of SK-HEP-1 hepatocellular carcinoma cells, JADE2 knockout provides a powerful tool to dissect the intersection of epigenetic regulation and cell cycle control in liver cancer. The loss of JADE2-mediated H4 acetylation likely leads to reduced transcription of replication-dependent genes, thereby attenuating uncontrolled proliferation. This model is instrumental for profiling histone modification landscapes, mapping HBO1 complex dependencies, and identifying JADE2-linked vulnerabilities. Furthermore, it allows for the examination of compensatory mechanisms or upstream signaling alterations that may arise upon disruption of the HBO1 axis in liver tumor cells.
Researchers can employ these polyclonal knockout cells in a wide array of assays, including western blotting for global H4 acetylation, RT-qPCR to quantify E2F target gene expression, and ChIP-qPCR to measure H4K5ac enrichment at specific loci. Flow cytometry with propidium iodide or EdU is suitable for cell cycle analysis, while MTT or BrdU proliferation assays evaluate growth kinetics. Transcriptomic profiling via RNA-seq complements the characterization of JADE2-dependent gene regulatory networks. This product is a versatile resource for epigenetic cancer biology, HBO1 complex studies, and functional genomics in hepatocellular carcinoma models. For technical inquiries, please contact Ascent Research.
