The HDGF Knockout SK-HEP-1 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal population of SK-HEP-1 human endothelial cells with targeted disruption of the hepatoma-derived growth factor (HDGF) gene. This loss-of-function model is designed for studying HDGF-dependent processes in a tumor-derived endothelial context. The polyclonal format provides a heterogeneous pool of knockout cells suitable for functional assays without requiring single-cell cloning.
The host SK-HEP-1 cell line was isolated from ascites of a patient with liver adenocarcinoma and displays an endothelial phenotype with vascular marker expression. It is a widely used model for tumor angiogenesis and the tumor microenvironment, particularly in hepatocellular carcinoma research. These cells retain functional properties of tumor-associated endothelial cells, including pro-angiogenic signaling and tube formation capacity, making them an ideal platform for dissecting endothelial gene functions in cancer.
HDGF is a pleiotropic growth factor that promotes cell proliferation, survival, and angiogenesis through extracellular receptor-mediated activation of the PI3K/Akt and MAPK/ERK pathways, employing kinases such as AKT1, MAPK3 (ERK1), and MAPK1 (ERK2). It is upregulated by transcription factors E2F1, Sp1, HIF-1??, and TGF-??, and downstream, HDGF induces CCND1, MYC, BIRC5, and VEGFA, along with matrix metalloproteinases MMP2 and MMP9. Intracellularly, HDGF interacts with nucleolin and PCNA, participates in ribosome biogenesis, and modulates transcriptional coactivators to support DNA repair and oncogenic growth. This places HDGF at a convergence point integrating mitogenic and stress signals.
In the SK-HEP-1 background, HDGF disruption enables focused study of its contribution to angiogenesis and liver cancer progression. Because SK-HEP-1 cells originate from a liver adenocarcinoma, knockout of HDGF is anticipated to impair angiogenic factor expression (e.g., VEGFA, MMPs) and attenuate endothelial-like responses, offering a clinically relevant model for hepatocellular carcinoma. The system also facilitates analysis of crosstalk within the tumor microenvironment and evaluation of anti-angiogenic therapy resistance.
Researchers can utilize these polyclonal knockout cells in diverse assays: Western blotting for protein validation, MTS/BrdU proliferation and Annexin V apoptosis assays for growth/survival phenotyping, Transwell migration and invasion assays for motility assessment, and tube formation assays for angiogenic capacity. Phospho-AKT and phospho-ERK analysis can probe signaling, while RNA-seq provides transcriptomic profiles. Xenograft models enable in vivo tumor growth studies. Applications include dissecting HDGF function in hepatocellular carcinoma, identifying angiogenesis mediators, validating HDGF as a drug target, and conducting functional genomics screens. For additional information, contact Ascent Research.
