The AGGF1 Knockout SK-HEP-1 Polyclonal Cells product is a CRISPR/Cas9-edited polyclonal knockout cell population derived from the SK-HEP-1 human hepatic adenocarcinoma line. These polyclonal cells harbor a targeted disruption of the AGGF1 gene, generated via CRISPR/Cas9-mediated gene editing, resulting in a heterogeneously edited population with loss-of-function potential for the encoded angiogenic factor. This model is designed for investigating AGGF1-dependent signaling in a hepatocellular carcinoma context characterized by endothelial-like properties, providing a versatile tool for both mechanistic studies and therapeutic screening.
The SK-HEP-1 cell line was originally established from the ascites of a patient with hepatic adenocarcinoma and is widely employed as an in vitro model of hepatocellular carcinoma. Notably, SK-HEP-1 cells exhibit endothelial-like characteristics, including the expression of certain endothelial markers and the capability for tube formation, which distinguishes them from typical epithelial tumor lines. This unique phenotype makes SK-HEP-1 an optimal platform for studying the convergence of tumor cell biology and angiogenic processes, particularly within the hepatic microenvironment.
AGGF1 encodes an angiogenic factor that promotes endothelial cell proliferation and migration by activating VEGFR2 signaling and enhancing DLL4-Notch pathway crosstalk. As a transcriptional activator, AGGF1 regulates genes critical for vascular development. Upstream regulators include GATA2, HIF1A, and VEGF, while downstream targets encompass VEGFR2, DLL4, and CDH5. AGGF1 directly interacts with VEGFR2, GATA2, and DLL4, thereby integrating VEGF-A/VEGFR2 signaling with DLL4-NOTCH1 pathway components such as NOTCH1, PI3K, AKT, and MAPK to coordinate angiogenic and transcriptional programs essential for vascular morphogenesis.
Disruption of AGGF1 in SK-HEP-1 cells creates a valuable loss-of-function model for dissecting the role of this angiogenic factor in a hepatocellular carcinoma background that retains intrinsic endothelial-like behavior. Given SK-HEP-1??s capacity for functional assays like tube formation and migration, the AGGF1 knockout population enables precise analysis of how loss of AGGF1 affects VEGFR2 phosphorylation, DLL4-Notch signaling dynamics, and downstream cellular phenotypes such as proliferation, motility, and network organization. This model is particularly relevant for elucidating the mechanistic interplay between tumor angiogenesis and transcriptional regulation in liver cancer.
Typical research applications for this knockout population include tumor angiogenesis research, hepatocellular carcinoma studies, anti-angiogenic drug testing, and endothelial cell biology. Researchers can employ these cells in a range of representative assays, including Western blotting, RT-qPCR, RNA-seq, tube formation assays, migration and proliferation assays, VEGFR2 phospho-analysis, co-immunoprecipitation, and immunofluorescence, to characterize AGGF1-dependent signaling networks and evaluate therapeutic interventions targeting the VEGF-A/VEGFR2/AGGF1/DLL4 axis. For additional information regarding this knockout model, please contact Ascent Research.
