The ACE2 Knockout SK-OV-3 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population derived from the SK-OV-3 human ovarian adenocarcinoma cell line, engineered to disrupt the ACE2 gene. This heterogeneous pool of cells exhibits a loss of ACE2 protein expression, providing a versatile loss-of-function model for investigating ACE2-dependent processes. The polyclonal format captures a range of knockout efficiencies across the population, suitable for applications where a mixed knockout background is desired, without requiring clonal isolation.
The parental SK-OV-3 cell line was established from the ascites of a 64-year-old Caucasian female with ovarian adenocarcinoma. These tumorigenic cells display epithelial morphology and serve as a well-established model for high-grade serous ovarian carcinoma, the most aggressive form of ovarian cancer. SK-OV-3 cells are widely used in oncology research to study tumor cell signaling, metastasis, and drug response. Their relevance to ovarian cancer pathophysiology makes them a pertinent host for examining the role of ACE2 in this malignancy.
ACE2 encodes a membrane-bound carboxypeptidase that cleaves angiotensin II into angiotensin-(1?C7), which activates the Mas receptor to counterbalance the renin?Cangiotensin system. This ACE2/Ang-(1?C7)/Mas axis promotes downstream Akt/eNOS signaling and nitric oxide production, mediating vasoprotective and anti-inflammatory effects. ACE2 activity is regulated by upstream factors such as inflammatory cytokines (TNF-??, IL-1??), interferons, and hypoxia. Crucially, ACE2 serves as the primary receptor for SARS-CoV-2 and SARS-CoV via direct binding of the viral spike protein, and it interacts with host factors including the B0AT1 transporter and ADAM17 sheddase.
In ovarian cancer, ACE2 is hypothesized to exert tumor-suppressive functions, potentially by modulating local angiotensin peptide levels and integrin signaling within the tumor microenvironment. The SK-OV-3 knockout model facilitates investigation of ACE2??s impact on cancer cell migration, invasion, and drug sensitivity. Additionally, these cells provide a native cancer-line background for studying SARS-CoV-2 entry mechanisms, eliminating the confounding effects of ectopic ACE2 overexpression commonly used in other cell models.
Key applications include Western blotting, RT-qPCR, and immunofluorescence for knockout validation; ACE2 enzymatic activity assays; pseudovirus entry assays to quantify spike protein-mediated internalization; and migration/invasion or drug sensitivity assays to evaluate functional consequences in ovarian cancer. The polyclonal pool supports co-immunoprecipitation of ACE2-interacting proteins such as spike protein. For technical inquiries, please contact Ascent Research.
