The ACE2 Knockout DLD-1 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal population derived from the DLD-1 colorectal adenocarcinoma line, designed for loss-of-function studies. The polyclonal pool contains cells with targeted disruptions in the ACE2 gene, preserving population heterogeneity while uniformizing knockout phenotype. This format avoids clonal artifacts and suits assays requiring bulk readouts, making it ideal for investigating ACE2 roles in cancer biology, viral entry, and cardiovascular signaling.
The parental DLD-1 cell line originates from a Duke??s type C colorectal adenocarcinoma and serves as a standard epithelial model for colorectal cancer research. DLD-1 cells harbor characteristic mutations in oncogenic pathways and are widely employed to study proliferation, migration, and drug response. Engineering ACE2 knockout in this background enables dissection of gene function within a colorectal tumor-relevant context.
ACE2 is a carboxypeptidase that converts Angiotensin II to Angiotensin 1-7, activating the Mas receptor to counterbalance AT1 receptor-mediated vasoconstriction and inflammation. Its expression is governed by upstream regulators including TNF-??, IL-1??, interferons, HIF-1??, SP1, AP-1, and microRNAs miR-421 and miR-200c. Downstream, Angiotensin 1-7 signals via Mas and AT2 receptors, leading to bradykinin release and amino acid transport through B0AT1. ACE2 also physically interacts with the SARS-CoV-2 spike protein, TMPRSS2, ADAM17, and collectrin, coupling viral entry mechanisms with RAS modulation.
In colorectal cancer, ACE2 likely influences tumor progression by modulating local RAS activity and amino acid transport, which are critical for tumor metabolism and microenvironment. DLD-1 cells are permissive to SARS-CoV-2 pseudovirus entry, so this knockout model aids in dissecting viral tropism and host?Cpathogen interactions in a gastrointestinal cancer setting. Additionally, ACE2 ablation allows examination of its impact on colorectal carcinoma proliferation, apoptosis resistance, and epithelial-to-mesenchymal transition.
Applications include SARS-CoV-2 pseudovirus entry assays, ACE2 enzymatic activity measurements, Western blotting, RT-qPCR, co-immunoprecipitation with TMPRSS2 or ADAM17, and angiotensin conversion assays. Migration, invasion, and drug sensitivity assays can reveal ACE2-dependent phenotypes in colorectal cancer. Immunofluorescence and flow cytometry enable surface receptor and signaling analysis. These tools facilitate research in virology, oncology, and cardiovascular biology. For further information, please contact Ascent Research.
