The ACE2 Knockout TE1 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal population derived from the TE1 cell line, featuring targeted disruption of the ACE2 gene. This heterogeneous knockout cell pool is generated without single-cell cloning, preserving cellular diversity while eliminating ACE2 expression, making it a robust model for studying ACE2-dependent processes.
The TE1 host cell line is a human esophageal squamous cell carcinoma line of epithelial origin, widely utilized in esophageal cancer research to investigate oncogenic signaling, drug resistance, and tumor biology. TE1 cells express components of the renin-angiotensin system (RAS) and are permissive to SARS-CoV-2 entry, providing a physiologically relevant context for examining ACE2 function in both cancer and viral infection.
ACE2 is a carboxypeptidase that converts angiotensin II to angiotensin-(1-7), which activates the Mas receptor to oppose the ACE/angiotensin II/AT1R axis. Angiotensin II is generated from angiotensinogen via renin and ACE, and binding to AT1R promotes proliferation and inflammation. ACE2-derived angiotensin-(1-7) triggers Mas receptor-mediated AKT and ERK signaling and nitric oxide production. ACE2 also serves as the receptor for SARS-CoV-2, with spike protein binding facilitated by TMPRSS2 and integrins, and complexes with B0AT1 for amino acid transport. Upstream regulators include angiotensin II, renin, glucocorticoids, IL-6, TNF-??, and hypoxia, while downstream factors encompass angiotensin-(1-7), Mas receptor, AKT, ERK, and nitric oxide.
In TE1 cells, ACE2 knockout disrupts the RAS balance, leading to elevated angiotensin II/AT1R signaling and reduced Mas receptor activation, potentially altering cell proliferation, migration, and inflammation, which can be evaluated using proliferation and migration assays. Loss of ACE2 also abolishes SARS-CoV-2 entry, enabling validation of viral host factors like TMPRSS2 in an esophageal cancer background. This model thus allows dissection of ACE2??s dual role in tumor suppression and viral susceptibility.
These polyclonal cells are suitable for mechanistic RAS studies, screening of ACE2-dependent anti-cancer agents, and SARS-CoV-2 infectivity research. Representative assays include Western blot and RT-qPCR for ACE2 and pathway markers, angiotensin peptide ELISA, viral pseudotype entry assay, and cell proliferation, migration, and invasion assays. The polyclonal population enhances experimental robustness and is ideal for high-throughput and detailed analyses. For more information, please contact Ascent Research.
