ACE Knockout A-549 Polyclonal Cells are a polyclonal population of human A-549 lung adenocarcinoma cells in which the ACE gene has been disrupted using CRISPR/Cas9. This heterogeneous loss-of-function model is ideal for studying ACE-dependent signaling without the variability of single-cell clones. The cells are supplied as a live, ready-to-use product for research in cancer biology, vascular biology, and infectious disease.
The parental A-549 cell line originated from a 58-year-old male lung adenocarcinoma patient. These adherent epithelial-like cells are a standard model for non-small cell lung cancer, retaining alveolar epithelial features and susceptibility to viral entry. Their well-characterized biology and expression of renin-angiotensin system components make them suitable for gene editing and functional assays.
ACE encodes a membrane-bound carboxypeptidase central to the renin-angiotensin system (RAS), catalyzing angiotensin I to angiotensin II conversion and bradykinin inactivation. Its expression is regulated by glucocorticoids, IL-1, endothelin-1, and TGF-??. Downstream, angiotensin II acts via AT1 and AT2 receptors to promote aldosterone secretion and cellular effects, while bradykinin signals through B2 receptors. ACE also interacts with calmodulin and forms heterodimers with ACE2, balancing RAS output. CRISPR/Cas9-mediated ACE disruption in these polyclonal cells leads to loss of enzymatic function, decreasing angiotensin II and increasing bradykinin levels.
In lung adenocarcinoma, ACE-derived angiotensin II can drive tumor progression through AT1 receptor-mediated proliferation, migration, and invasion. Knocking out ACE in A-549 cells provides a model to dissect local RAS contributions to non-small cell lung cancer and explore compensatory mechanisms involving ACE2. Additionally, because ACE and ACE2 are receptors for coronaviruses, this knockout is valuable for studying SARS-CoV-2 infection dynamics and the ACE/ACE2 balance in viral entry. These applications extend to investigating therapeutic strategies for cancer and COVID-19-related acute respiratory distress syndrome.
This polyclonal knockout product supports diverse assays: Angiotensin II ELISA and ACE activity assays to confirm functional ablation; RT-qPCR and Western blotting for gene and protein analysis; proliferation, migration, and invasion assays to assess tumor cell behavior; and drug sensitivity testing with ACE inhibitors or angiotensin receptor blockers. Flow cytometry can monitor surface receptor changes. The model also enables SARS-CoV-2 spike protein interaction studies. For further information, contact Ascent Research.
