The EDIL3 Knockout SK-HEP-1 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal cell population derived from the human hepatic adenocarcinoma cell line SK-HEP-1, engineered for loss-of-function studies of the EDIL3 gene. This polyclonal knockout product introduces targeted gene disruption using CRISPR/Cas9 technology, generating a heterogeneous pool of cells with EDIL3 ablation, enabling robust functional analyses without selection of a single clone. The population retains the parental SK-HEP-1 background while eliminating EDIL3-encoded Del-1 protein expression, providing a physiologically relevant system to dissect EDIL3-mediated signaling in liver cancer and endothelial biology contexts.
The SK-HEP-1 host cell line is widely employed as a model for hepatocellular carcinoma and endothelial cell behavior due to its dual expression of hepatic and endothelial markers. Originally isolated from a patient with liver adenocarcinoma, SK-HEP-1 cells exhibit anchorage-independent growth, invasive capacity, and the ability to form capillary-like structures in vitro, making them exceptionally suitable for investigating tumor angiogenesis, metastasis, and cell?Cmatrix interactions. Their genetic background and robust growth characteristics facilitate reproducible CRISPR-based engineering and downstream phenotypic assays.
EDIL3 encodes the secreted glycoprotein Del-1, which functions as a matricellular ligand for integrin receptors ??v??3 and ??v??5. Upon integrin binding, Del-1 activates focal adhesion kinase (FAK) and its downstream effectors Akt, ERK, and NF-??B, orchestrating cell adhesion, migration, survival, and angiogenic programs. EDIL3 expression is induced by VEGF, TNF-??, IL-1??, and hypoxic conditions through HIF-1??, linking extracellular stimuli to intracellular signaling cascades. The EDIL3?Cintegrin?CFAK?CAkt axis is a critical node in the regulation of endothelial cell dynamics and inflammatory responses, with Del-1 also interacting with phosphatidylserine to modulate phagocytosis and immune cell recruitment.
In SK-HEP-1 cells, endogenous EDIL3 contributes to the oncogenic and pro-angiogenic phenotype by sustaining integrin-mediated adhesion and activation of FAK/Akt/ERK pathways. CRISPR/Cas9-mediated disruption of EDIL3 in these cells eliminates Del-1 production, thereby impairing integrin-directed focal adhesion assembly, haptotactic migration, and tube formation capacity. This knockout model also dampens NF-??B-driven inflammatory signaling, offering a unique platform to study the interplay between liver cancer cells, the vasculature, and the immune microenvironment. Attenuation of EDIL3 signaling in SK-HEP-1 cells mirrors aspects of reduced tumor vascularization and metastatic spread observed in preclinical models, positioning this product as a powerful tool for mechanistic dissection.
Researchers can employ this polyclonal knockout population in functional assays: Matrigel tube formation for angiogenic potential, Transwell migration/invasion for metastatic behavior, and cell adhesion on integrin substrates. Signaling readouts include western blotting for phospho-FAK, phospho-Akt, and phospho-ERK, alongside RT-qPCR for angiogenic factors (e.g., VEGF, angiopoietin-2). Immunofluorescence for focal adhesion proteins and flow cytometry for apoptosis provide additional phenotypic insight, supporting drug screening for EDIL3/integrin axis inhibitors and novel anti-invasive agents. For further information or technical support, please contact Ascent Research.
