The EGFL7 Knockout HGC-27 Polyclonal Cells constitute a CRISPR/Cas9-edited polyclonal knockout population generated from the human gastric carcinoma cell line HGC-27. This product provides a heterogeneous pool of HGC-27 cells carrying targeted disruptions in the EGFL7 gene, resulting in loss of functional EGFL7 protein expression. As a polyclonal knockout model, it recapitulates the genetic diversity inherent to CRISPR-edited populations, making it suitable for functional studies where clonal variation is not a primary concern.
The HGC-27 cell line was originally established from the lymph node metastasis of an undifferentiated gastric carcinoma and exhibits an epithelial morphology. It serves as a well-characterized in vitro model for metastatic gastric cancer, retaining hallmark genetic and phenotypic features of aggressive disease. The cells are proficient in invasion and have been widely used to investigate the molecular mechanisms of gastric cancer metastasis, including epithelial-mesenchymal transition (EMT), cell motility, and tumor-stroma interactions.
EGFL7 encodes a secreted angiogenic factor that regulates vascular tube formation and endothelial cell migration. Its expression is induced by HIF-1??, VEGF, and TGF-??1. Secreted EGFL7 interacts with Notch receptors Notch1 and Notch4 and with integrin ??v??3/fibronectin complexes, activating downstream PI3K/Akt signaling. Within the angiogenic pathway, EGFL7 cooperates with Dll4, VEGF, VEGFR2, and Akt. EGFL7 promotes angiogenesis by modulating Notch and integrin signaling, enhancing endothelial cell survival and tube formation.
In the context of HGC-27 gastric adenocarcinoma cells, EGFL7 is implicated in promoting a pro-angiogenic and pro-metastatic tumor microenvironment. Disruption of EGFL7 in this cell line provides a valuable loss-of-function model to investigate its contributions to gastric cancer progression, particularly in regulating endothelial cell recruitment, vascular remodeling, and metastatic dissemination. The polyclonal knockout population allows assessment of EGFL7-dependent phenotypes in a bulk setting, reflecting the heterogeneity of tumor cell populations observed in vivo.
Researchers can employ this knockout model for western blotting and RT-qPCR to confirm gene disruption and assess signaling changes, as well as tube formation, migration, and invasion assays to study angiogenesis and cell motility. In vivo xenograft assays combined with immunohistochemistry for angiogenesis markers enable evaluation of EGFL7??s role in tumor vascularization and metastasis. This tool is particularly valuable for drug target validation of anti-angiogenic therapies in gastric cancer. For additional information, please contact Ascent Research.
