The ADIPOR1 Knockout A-549 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population derived from the A-549 human lung adenocarcinoma cell line, featuring targeted disruption of the ADIPOR1 gene. This heterogeneous knockout pool avoids clonal selection bias and provides a robust model for studying adiponectin receptor 1 function in lung cancer biology, metabolic regulation, and drug response.
The parental A-549 cell line was established from a 58-year-old male patient with lung adenocarcinoma and displays features of alveolar epithelial type II cells. It serves as a widely accepted in vitro system for investigating alveolar epithelial barrier integrity, viral entry, and drug metabolism. This well-characterized lung cancer model supplies a biologically relevant host context for examining ADIPOR1-mediated signaling pathways.
The ADIPOR1 gene encodes a high-affinity receptor for adiponectin. Ligand binding recruits APPL1, activating AMPK??1/??2, which phosphorylates and inhibits ACC, thus boosting fatty acid oxidation. Simultaneously, ADIPOR1 stimulates PPAR?? transcriptional activity, upregulating GLUT4 to promote glucose uptake. The receptor also exerts intrinsic ceramidase activity, reducing ceramide levels to improve insulin sensitivity and dampen NF-??B-driven inflammation. ADIPOR1 expression is regulated by PPAR?? agonists, insulin, fatty acids, and cytokines such as TNF-?? and IL-6, positioning it at the intersection of metabolic and inflammatory signaling.
In A-549 lung adenocarcinoma cells, ADIPOR1 disruption permits detailed analysis of adiponectin-dependent metabolic reprogramming, including changes in glucose consumption and lipid metabolism that are often dysregulated in cancer. This knockout model enables investigation of ADIPOR1??s contributions to insulin sensitization and anti-inflammatory pathways within a malignant epithelial environment. Furthermore, leveraging the A-549 background??s relevance to drug metabolism, researchers can explore how ADIPOR1 signaling modulates chemosensitivity and resistance, offering potential insights into therapeutic vulnerabilities.
This polyclonal knockout cell product is well-suited for diverse functional assays: western blotting and RT-qPCR can confirm ADIPOR1 loss; immunofluorescence and flow cytometry allow assessment of receptor distribution; glucose uptake and fatty acid oxidation assays quantify metabolic changes; co-immunoprecipitation and phospho-AMPK analysis enable study of protein interactions and pathway activation; and migration and drug sensitivity assays reveal effects on metastasis and therapy response. For further information, please contact Ascent Research.
