The HEG1 Knockout SK-HEP-1 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal cell population derived from the SK-HEP-1 human liver adenocarcinoma cell line, designed for loss-of-function studies of the HEG1 gene. As a polyclonal knockout model, this product provides a genetically diverse cell pool that avoids clonal selection bias, enabling robust assessment of HEG1-dependent phenotypes. The cell population is suitable for a broad range of biomedical research applications, including cancer biology, vascular biology, and drug discovery.
SK-HEP-1 is a unique cell line originating from the ascitic fluid of a patient with liver adenocarcinoma. It is characterized by co-expression of epithelial and endothelial markers, making it a valuable model for hepatocellular carcinoma with endothelial-like features. This dual phenotype facilitates the study of both tumor cell behavior and endothelial functions, such as barrier integrity and angiogenesis, within a single cellular context. Its endothelial characteristics are particularly relevant for investigating HEG1-mediated adhesion processes.
HEG1 encodes a transmembrane receptor that functions through interaction with the receptor-type protein tyrosine phosphatase PTPRM. Mechanistically, HEG1 binding to PTPRM promotes stabilization of VE-cadherin/??-catenin complexes at adherens junctions, a critical step in maintaining endothelial cell?Ccell adhesion. Upstream regulators include the transcription factors GATA4, TBX5, and MEF2C, as well as mechanical shear stress. Downstream, HEG1 signaling influences VE-cadherin, ??-catenin, p120-catenin, and the actin cytoskeleton, and intersects with the Notch pathway through components such as Notch1 and DLL4, as well as VEGFR2 in VEGF signaling.
Disruption of HEG1 expression in SK-HEP-1 cells leads to compromised junctional integrity, resulting in increased endothelial permeability, enhanced cell migration, and invasive behavior. These phenotypic changes mirror key processes in cancer metastasis and congenital cardiovascular defects, such as ventricular septal defects. The polyclonal knockout model thus provides a physiologically relevant system for dissecting the molecular mechanisms that underpin vascular dysfunction and tumor cell dissemination.
This product is well-suited for a wide array of experimental techniques, including Western blotting and immunofluorescence staining for adhesion proteins, endothelial permeability assays, and Transwell migration/invasion assays. Co-immunoprecipitation can be employed to examine the HEG1?CPTPRM complex, while qRT-PCR and flow cytometry enable quantification of gene expression and surface receptor levels. In vivo, xenograft tumor growth assays can assess metastatic potential. These applications support drug targeting studies, angiogenesis research, and functional analysis of cell adhesion pathways. For further information or technical support, please contact Ascent Research.
