The ACE2 Knockout Ca Ski Polyclonal Cells constitute a CRISPR/Cas9-edited polyclonal knockout cell population derived from the Ca Ski human cervical carcinoma cell line. This product is designed to disrupt the ACE2 gene, generating a mixed population of cells with heterogeneous knockout alleles. The polyclonal format provides a robust model for studying ACE2 loss-of-function without the bottlenecks associated with single-cell cloning. This knockout cell population serves as a versatile tool for investigating ACE2-dependent signaling and its roles in viral entry and cancer biology.
Ca Ski cells are an adherent epithelial cell line established from a cervical epidermoid carcinoma and harbor integrated human papillomavirus type 16 (HPV-16) genomes. They represent a widely used model for malignant cervical epithelial cell biology, reflecting features of HPV-driven carcinogenesis. The retention of epithelial characteristics and tumorigenic potential makes Ca Ski cells suitable for exploring gene function in the context of cervical cancer, including studies of invasion, migration, and drug response.
ACE2 encodes a carboxypeptidase that converts angiotensin II to angiotensin-(1-7), which activates the Mas receptor to promote vasodilation, anti-fibrotic, and anti-inflammatory effects. ACE2 is also the primary cellular receptor for SARS-CoV and SARS-CoV-2 spike proteins, mediating viral entry. Within the renin-angiotensin system, ACE2 counterbalances ACE activity. Upstream regulators include angiotensin II, IL-1??, HNF1??, and estrogen, while downstream targets comprise angiotensin-(1-7), AKT, and eNOS. ACE2 interacts with SARS-CoV-2 spike protein, SLC6A19 (B0AT1), and integrin ??1. Disruption of ACE2 in Ca Ski cells permits dissection of these molecular interactions.
In Ca Ski cervical carcinoma cells, ACE2 knockout enables investigation of how the renin-angiotensin system intersects with HPV-associated malignancy. Since ACE2 may influence cell proliferation, migration, and inflammatory responses, this polyclonal knockout population provides a platform to assess the impact of ACE2 loss on cancer-related phenotypes. Additionally, because Ca Ski cells express epithelial markers, they offer a relevant system to study ACE2-mediated SARS-CoV-2 entry mechanisms in an epithelial context, potentially revealing insights into viral tropism and host susceptibility.
Researchers can employ this knockout model in a variety of functional assays, including Western blotting, RT-qPCR, and flow cytometry to confirm ACE2 disruption. Angiotensin II conversion assays quantify enzymatic activity loss, while SARS-CoV-2 pseudovirus entry assays directly measure viral uptake. Migration assays further allow evaluation of ACE2??s role in cellular motility. Applications span SARS-CoV-2 infection studies, renin-angiotensin system analysis, cardiovascular disease modeling, and cancer biology research. For further product inquiries, please contact Ascent Research.
