The ANGPTL4 Knockout A-549 Polyclonal Cells constitute a CRISPR/Cas9-edited polyclonal knockout population derived from the A-549 human lung carcinoma cell line. This product features heterogeneous disruption of the ANGPTL4 gene, providing a bulk-edited cell pool suitable for population-level functional studies. The polyclonal format avoids clonal selection bias and preserves genetic heterogeneity, making it ideal for pathway dissection and drug screening applications.
A-549 is an adherent epithelial cell line established from a 58-year-old Caucasian male with lung cancer. It serves as a widely used model for lung adenocarcinoma and type II pneumocyte biology. These cells express relevant integrins and metabolic regulators, establishing a native background for investigating ANGPTL4 functions in lipid metabolism and cancer cell behavior.
ANGPTL4 is a secreted inhibitor of lipoprotein lipase (LPL) that governs triglyceride clearance and systemic lipid handling. Its expression is induced by PPAR??, PPAR??, HIF-1??, TGF-??, insulin, and TNF-??. In malignancy, ANGPTL4 engages integrins ??5??1 and ??v??3, as well as vitronectin and fibronectin, to activate focal adhesion kinase (FAK). FAK stimulates PI3K/Akt and ERK1/2 pathways, leading to NF-??B activation, thereby driving migration, invasion, and angiogenesis. ANGPTL4 also interacts with ANGPTL3 and ANGPTL8 to coordinate lipid and adhesion signaling.
In A-549 cells, ANGPTL4 knockout disrupts LPL inhibition and integrin-FAK signaling, potentially altering lipid metabolism and attenuating pro-invasive networks. This model is highly relevant for studying the intersection of metabolic syndrome and lung adenocarcinoma progression, as ANGPTL4 contributes to both systemic lipid dysregulation and epithelial-mesenchymal transition within the lung epithelial milieu.
Applications include lipid metabolism studies (LPL activity assays), metastasis research (Transwell migration, Matrigel invasion), angiogenesis (tube formation), drug target validation, and metabolic disease modeling. ANGPTL4 disruption can be verified by western blotting or RT-qPCR, and downstream signaling examined via phospho-FAK immunoblotting or RNA-seq. For further details and technical support, please contact Ascent Research.
