The GXYLT1 Knockout SK-HEP-1 Polyclonal Cells consist of a CRISPR/Cas9-mediated gene-disrupted polyclonal cell population targeting the GXYLT1 locus in the human SK-HEP-1 hepatic adenocarcinoma cell line. This product provides a loss-of-function model to dissect GXYLT1-dependent xylosyltransferase activity and its impact on Notch signaling. The polyclonal knockout format retains population heterogeneity, offering a robust tool for functional studies without the confounding effects of clonal selection, making it ideal for investigating glycosylation-dependent Notch signaling in hepatocellular carcinoma.
SK-HEP-1 is a male-derived, ascites-sourced hepatic adenocarcinoma cell line commonly employed in hepatocellular carcinoma (HCC) research. It exhibits adherent morphology and retains tumorigenic properties, including anchorage-independent growth and migration, making it a standard in vitro model for HCC. Its endogenous Notch pathway activity and widespread use in drug discovery and mechanistic studies ensure compatibility with established assays and literature.
GXYLT1 encodes a xylosyltransferase that catalyzes xylose addition to O-glucose on Notch EGF repeats, following O-glucosylation by POGLUT1. This modification fine-tunes Notch receptor processing by modulating ligand affinity and receptor stability. Upon DLL/JAG ligand binding, Notch receptors undergo gamma-secretase cleavage, releasing NICD. NICD forms a complex with RBPJ and MAML coactivators to transcriptionally regulate targets such as HES1 and HEY1. GXYLT1 disruption is expected to attenuate NICD generation and downstream gene expression, influencing proliferation and migration.
In HCC, Notch signaling can promote or suppress tumorigenesis depending on cellular and microenvironmental context. GXYLT1 knockout in SK-HEP-1 cells allows direct assessment of how O-glucose xylosylation impacts Notch-dependent transcriptional programs and phenotypic outcomes including proliferation, invasion, and survival. This genetically defined model helps dissect glycosylation-dependent signaling networks in liver cancer, potentially uncovering therapeutic vulnerabilities that target Notch regulatory mechanisms.
These polyclonal knockout cells are suitable for a range of functional and biochemical assays, including Western blot analysis of GXYLT1 and NICD, RT-qPCR of HES1/HEY1, Notch luciferase reporter assays, transwell migration/invasion, MTT proliferation, and immunofluorescence. Together, these enable comprehensive characterization of GXYLT1 function in HCC signaling networks. For further information, please contact Ascent Research.
