The ANPEP Knockout A-549 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population derived from the human A-549 lung adenocarcinoma epithelial cell line. This product features targeted disruption of the ANPEP gene, which encodes aminopeptidase N (CD13), thereby eliminating functional ANPEP expression. The polyclonal format retains genetic diversity inherent in a pool of edited cells, providing a robust loss-of-function model for studying CD13-dependent processes without clonal selection bias.
The parental A-549 cell line was established from explanted human lung adenocarcinoma tissue and exhibits an adherent epithelial morphology. These cells harbor a KRAS G12S activating mutation while maintaining wild-type TP53 status, making them a well-characterized model for non-small cell lung carcinoma research. A-549 cells are widely used in respiratory epithelial barrier studies, cancer drug testing, and investigations into tumor cell invasion and metastasis due to their consistent growth and retention of key oncogenic pathways.
ANPEP encodes a type II transmembrane zinc-dependent aminopeptidase that cleaves N-terminal neutral amino acids from peptides, modulating bioactive molecules such as angiotensin peptides and extracellular matrix components. CD13 is transcriptionally upregulated by TNF-alpha, IFN-gamma, and hypoxia-inducible factors. Downstream, ANPEP promotes integrin beta-1 (ITGB1)-mediated adhesion to collagen and fibronectin, and facilitates focal adhesion kinase (FAK) and ERK1/2 phosphorylation to drive migration and angiogenesis. Additionally, CD13 interacts with MMP-2 to aid matrix degradation, and its activity potentiates VEGF signaling, linking aminopeptidase function to angiogenic and metastatic cascades.
Within the A-549 context, ANPEP knockout disrupts these interconnected pathways, providing a tool to dissect its role in lung adenocarcinoma progression. Loss of CD13 impairs angiotensin processing, reduces integrin-dependent adhesion and migration, and attenuates pro-angiogenic ERK1/2 signaling. This model enables precise examination of how ANPEP contributes to the malignant phenotype of KRAS-mutant lung epithelial cells, including invasion capacity and endothelial tube formation stimulation.
The ANPEP Knockout A-549 Polyclonal Cells are suitable for lung cancer invasion and metastasis assays, angiogenesis studies, drug resistance screening, and peptide substrate profiling. Researchers can employ Transwell migration, Matrigel invasion, phospho-ERK1/2 analysis, and aminopeptidase activity measurements. Additional applications include viral entry receptor studies, tumor microenvironment interactions, and drug sensitivity profiling, making this a versatile resource for oncology and cell biology. For further information, please contact Ascent Research.
