The EGFL7 Knockout HeLa Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population designed as a loss-of-function model for studying EGFL7 biology. This heterogeneous pool of knockout cells, generated by CRISPR/Cas9-mediated genome editing, allows investigation of EGFL7-dependent processes at the population level, suitable for functional assays that do not require clonal isolation, and provides a robust platform for exploring EGFL7 signaling in a cervical cancer context.
The host cell line is HeLa, a cervical adenocarcinoma-derived cell line positive for HPV18. HeLa cells exhibit an epithelial-like morphology and are widely used in cancer biology, signal transduction, and drug discovery due to their robust proliferation and well-characterized genome. Introducing EGFL7 knockout into HeLa creates a clinically relevant system to study the role of this secreted factor in tumor cell behavior and angiogenesis-related signaling.
EGFL7 is a secreted endothelial cell-derived factor critical for angiogenesis and vascular tube formation. It binds integrin ??v??3 (ITGAV/ITGB3) and modulates Notch signaling via interaction with NOTCH1 and heparan sulfate proteoglycans, leading to activation of FAK (PTK2), AKT1, and ERK1/2 (MAPK3/MAPK1) phosphorylation, and induction of Notch targets HES1 and HEY1. Upstream, EGFL7 is regulated by HIF1A, VEGFA, and NICD, positioning it at the nexus of angiogenic and survival pathways.
In HeLa cells, EGFL7 is endogenously expressed and may function autocrinely to modulate adhesion, migration, and survival. Its disruption in this polyclonal population enables dissection of contributions to cervical adenocarcinoma cell invasiveness and angiogenic responses. Since HeLa cells do not form vascular structures, the knockout model is valuable for generating conditioned media to study paracrine effects on endothelial cells, e.g., tube formation with HUVECs. Loss of EGFL7 potentially alters integrin signaling and cross-talk with Notch and PI3K/AKT pathways, offering insights into vascular malformations and tumor angiogenesis.
This knockout product supports functional analysis of EGFL7 in cervical cancer, angiogenesis research, and Notch signaling studies. Representative assays include Western blotting and RT-qPCR, scratch wound migration, Boyden chamber invasion, tube formation using conditioned media on HUVECs, Notch reporter, integrin activation, and phospho-AKT/ERK immunoblotting. The polyclonal format facilitates rapid functional screening without clonal selection, enabling high-throughput tumor biology and drug response studies. For further information, contact Ascent Research.
