The ACE2 Knockout LoVo Polyclonal Cells are a pooled population of LoVo cells subjected to CRISPR/Cas9-mediated disruption of the ACE2 gene. This product provides a heterogeneous polyclonal knockout model, obviating the need for single-cell cloning while enabling efficient evaluation of ACE2-dependent functions. The polyclonal format preserves population-level diversity and is well-suited for experiments requiring rapid generation of ACE2-deficient cells without the clonal selection bottleneck.
The parental LoVo cell line is an adherent epithelial line derived from a metastatic lymph node of a human colorectal adenocarcinoma. These cells are tumorigenic and express carcinoembryonic antigen (CEA), reflecting their origin from metastatic colorectal cancer. LoVo cells are widely used as a model system for studying colorectal adenocarcinoma biology, drug responses, and interactions with infectious agents such as SARS-CoV-2.
ACE2 encodes a carboxypeptidase that serves as the entry receptor for SARS-CoV and SARS-CoV-2, binding the spike glycoprotein with the co-factor TMPRSS2. In the renin-angiotensin system, ACE2 converts angiotensin II to angiotensin 1-7, which acts on the MAS1 receptor to counterbalance vasoconstrictive and inflammatory signaling. ACE2 expression is upregulated by interferon-gamma (IFNG), tumor necrosis factor-alpha (TNF), hypoxia-inducible factor 1-alpha (HIF1A), and hepatocyte nuclear factor 1-alpha (HNF1A), while angiotensin II itself can modulate its levels. Key downstream mediators include angiotensin 1-7 and bradykinin, with consequences for inflammatory cytokine production. ACE2 also interacts with solute carrier SLC6A19 and integrins, linking it to amino acid transport and cell adhesion.
In the LoVo colorectal adenocarcinoma context, disruption of ACE2 eliminates the critical host factor needed for SARS-CoV-2 infection, rendering the cells resistant to viral entry. Simultaneously, loss of ACE2 activity impairs the local conversion of angiotensin II to angiotensin 1-7, thereby altering the balance of renin-angiotensin system signaling. This imbalance can affect tumor cell proliferation, apoptosis, and inflammation, making the knockout cells a valuable tool to dissect the contribution of ACE2 to colorectal cancer progression and the interplay between cancer biology and COVID-19 susceptibility.
This polyclonal knockout model supports studies of SARS-CoV-2 host cell entry, ACE2 signaling, and renin-angiotensin system function in colorectal cancer. Applications include antiviral drug screening, host factor analysis, and functional genomics using assays such as pseudovirus entry, angiotensin II conversion, Western blotting, immunofluorescence, RT-qPCR, and RNA sequencing. For further details or assistance, please contact Ascent Research.
