The EGFL7 Knockout Huh-7 Polyclonal Cells product is a CRISPR/Cas9-edited polyclonal cell population derived from the Huh-7 human hepatocellular carcinoma cell line, harboring a targeted disruption of the EGFL7 gene. This polyclonal pool enables loss-of-function studies of EGFL7 without requiring single-cell cloning, maintaining genetic diversity while abolishing EGFL7 expression. As a mixed population, it reflects a more physiologically relevant model for interrogating EGFL7 function compared to monoclonal isolates, and is suitable for a broad range of functional assays.
Huh-7 cells are a well-differentiated hepatocellular carcinoma cell line originally established from a liver tumor of a 57-year-old Japanese male. These cells retain many hepatocytic features and are widely employed in hepatocellular carcinoma research, including studies of tumor cell proliferation, invasion, and drug responses. Their extensive characterization and compatibility with various molecular biology techniques make them an ideal host for genetic perturbation experiments investigating liver cancer biology.
EGFL7 (Epidermal Growth Factor-like domain-containing protein 7) is a secreted angiogenic factor predominantly studied in vascular development and tumor angiogenesis. Mechanistically, EGFL7 binds to integrin ??v??3, leading to phosphorylation of FAK (PTK2) and activation of the PI3K/AKT1 signaling cascade, thereby promoting endothelial cell migration and capillary-like tube formation. Additionally, EGFL7 interacts with NOTCH1 and modulates NOTCH signaling, a critical pathway in vascular morphogenesis. Upstream, EGFL7 expression is regulated by VEGFA, HIF1A, and TGFB1. Downstream effectors include MAPK1/3 (ERK1/2) in addition to AKT1, indicating crosstalk with the Ras-MAPK pathway. Representative pathway components such as VEGFR2, SRC, DLL4, and ITGB3 further situate EGFL7 within a signaling network essential for angiogenesis and tumor progression.
In the context of hepatocellular carcinoma, EGFL7 has been implicated in promoting tumor growth and metastasis through its pro-angiogenic and integrin-mediated activities. Huh-7 cells endogenously express EGFL7, making them a relevant model system for exploring its roles in liver cancer cell migration, invasion, and interactions with the tumor microenvironment. By abrogating EGFL7 function in this polyclonal Huh-7 population, researchers can dissect the contribution of EGFL7 to HCC-specific phenotypes, including resistance to anti-angiogenic therapies and integrin-dependent signaling alterations.
This knockout cell product is ideally suited for angiogenesis research, hepatocellular carcinoma metastasis studies, and integrative analysis of integrin and NOTCH signaling cascades. Typical applications include Transwell migration assays and wound healing assays to measure cell motility, as well as tube formation assays with conditioned media to assess paracrine angiogenic activity. Downstream signaling events can be scrutinized by phospho-AKT (Ser473) and phospho-FAK (Tyr397/925) western blotting, while physical interactions between EGFL7 and integrins can be examined using co-immunoprecipitation and immunofluorescence staining. The product also supports drug resistance investigations and tumor microenvironment interaction studies under defined experimental conditions. For additional information, please contact Ascent Research.
