The EGFL7 Knockout A-549 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population derived from the A-549 human lung epithelial carcinoma cell line. This product provides a heterogeneous pool of cells harboring targeted disruption of the EGFL7 gene, creating a versatile loss-of-function model system. The polyclonal format allows researchers to investigate EGFL7 function without the clonal selection artifacts often associated with single-cell-derived knockout lines, offering a more representative population for studying heterogeneous cancer cell behavior.
Host A-549 cells were originally established from the lung adenocarcinoma of a 58-year-old Caucasian male and exhibit adherent epithelial morphology with features of type II alveolar epithelial cells. This cell line is widely utilized in cancer and respiratory disease research due to its stable growth characteristics and relevance to non-small cell lung cancer (NSCLC) biology. A-549 cells express key oncogenic drivers and are frequently employed to study tumor cell proliferation, migration, invasion, and drug response, making them a suitable background for EGFL7 knockout studies.
EGFL7 is a secreted extracellular matrix protein that functions primarily in the vasculature by modulating endothelial cell migration and vascular tube formation. Mechanistically, EGFL7 interacts with integrins such as ITGAV and ITGB3, and with Notch receptors including NOTCH1 and DLL4, thereby influencing cell adhesion, motility, and angiogenic signaling. The protein is transcriptionally regulated by upstream factors VEGFA and HIF1A, while downstream signaling involves phosphorylation of FAK (PTK2) and AKT1. In the Notch pathway, EGFL7 impacts signaling through NOTCH1, its ligand DLL4, and downstream effectors such as JAG1 and HES1. Through these interactions, EGFL7 coordinates extracellular matrix organization and drives angiogenesis, processes frequently dysregulated in cancer.
Within the A-549 lung adenocarcinoma context, disruption of EGFL7 provides a powerful tool to dissect its contributions to tumor cell adhesion, migration, and metastatic dissemination. Given the established role of EGFL7 in promoting angiogenesis, this knockout model is particularly valuable for investigating tumor?Cmicroenvironment crosstalk and the impact of tumor-derived EGFL7 on endothelial cell behavior. Moreover, the polyclonal knockout population enables examination of EGFL7-dependent phenotypes in a genetically diverse setting, reflecting the intratumoral heterogeneity observed in clinical lung cancers.
This knockout product is well-suited for a broad range of functional assays, including wound healing and cell adhesion assays to quantify migratory and adhesive capacity, tube formation assays in co-culture with endothelial cells to assess angiogenic potential, and molecular analyses such as Western blotting, RT-qPCR, and immunofluorescence to confirm target-gene disruption and explore signaling networks. Research applications extend to cancer metastasis studies, drug target validation, tumor microenvironment characterization, and vascular biology investigations. For further information or to request a quote, please contact Ascent Research.
