The ACE2 Knockout MCF-7 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal cell population with disruption of the human ACE2 gene in the MCF-7 breast adenocarcinoma line. This loss-of-function model provides a heterogeneous pool of knockout cells generated without single-cell cloning, reducing clonal artifacts and enabling robust assessment of ACE2-dependent processes in an epithelial context. The polyclonal format supports pooled analyses and population-level studies, making it suitable for routine gene function interrogation.
MCF-7 cells, derived from a pleural effusion of a metastatic breast adenocarcinoma patient, are estrogen receptor-positive and serve as a standard model for estrogen-responsive breast cancer. They retain luminal subtype characteristics, including functional estrogen receptor signaling and hormonal responsiveness, and are widely used in hormone-dependent tumorigenesis assays, anti-estrogen drug screening, and epithelial cell signaling studies. Their well-documented growth and invasion properties provide a reliable host for knockout modeling of gene candidates in breast cancer biology.
ACE2 is a zinc carboxypeptidase and the primary receptor for SARS coronaviruses. It converts angiotensin II to angiotensin-(1-7), which acts via the Mas receptor to induce vasodilation, anti-inflammatory, and anti-fibrotic effects. ACE2 also partners with B0AT1 for amino acid transport. Its expression is regulated by interferons, HIF-1??, FOXO1, and glucocorticoids, while ADAM17 and TMPRSS2 mediate ectodomain shedding. Downstream, ACE2/angiotensin-(1-7) signaling enhances nitric oxide synthase activity, increases IL-10, and reduces TGF-?? levels. This positions ACE2 as a key integrator of the renin-angiotensin system with implications for inflammation, fibrosis, and viral entry.
In MCF-7 cells, ACE2 knockout eliminates both enzymatic conversion of angiotensin II and SARS-CoV-2 receptor function, leading to elevated angiotensin II and loss of angiotensin-(1-7)-mediated signaling. This may perturb the balance between proliferative and anti-proliferative pathways, particularly given potential crosstalk with estrogen receptor signaling. The model allows dissection of ACE2??s role in tumor cell behavior, including proliferation and migration, and its impact on the tumor microenvironment, through effects on angiotensin peptide levels and interactions with B0AT1 and integrins.
Applications include SARS-CoV-2 pseudovirus entry assays, ACE2 activity measurements via angiotensin peptide ELISA, and signaling studies using Western blot or RT-qPCR for downstream targets. The cells are suitable for drug target validation within the renin-angiotensin system and for tumor microenvironment investigations, such as cell migration assays. RNA-seq-based transcriptomics can further delineate global expression changes upon ACE2 disruption. These polyclonal knockout cells offer a flexible platform for ACE2 research in breast cancer and virology. For further information, contact Ascent Research.
