The DNPEP Knockout MES-OV Polyclonal Cells product comprises a CRISPR/Cas9-edited polyclonal population of MES-OV human ovarian carcinoma cells with targeted disruption of the DNPEP gene, which encodes aspartyl aminopeptidase. Generated without single-cell cloning, this heterogeneous knockout pool provides a versatile loss-of-function model for studying DNPEP in cancer biology.
The MES-OV cell line is derived from a human ovarian carcinoma and is widely used to investigate ovarian cancer pathogenesis, including proliferation, invasion, and drug response. Its epithelial morphology and tumorigenic properties make it suitable for in vitro and xenograft studies of oncogenic signaling.
DNPEP encodes a zinc-dependent exopeptidase that cleaves N-terminal aspartate and glutamate residues from peptides, notably catalyzing the conversion of angiotensin II to angiotensin III within the renin-angiotensin system. Its expression is regulated by STAT3, NF-??B, and angiotensin II, while its activity modulates downstream AT1 and AT2 receptor signaling. By generating angiotensin III, DNPEP shifts the balance from pro-hypertensive and mitogenic AT1R pathways toward AT2R-mediated effects, thereby influencing vasoconstriction, salt homeostasis, and cellular proliferation.
In the ovarian cancer context, DNPEP disruption may attenuate angiotensin II-induced oncogenic signaling, impairing cell growth, migration, and angiogenesis. Moreover, this model can be employed to study crosstalk between RAS and other proliferative pathways, such as those driven by STAT3 and NF-??B, which are known upstream regulators of DNPEP. Since MES-OV cells express RAS components, this knockout platform enables dissection of local peptide metabolism and its impact on tumor progression, offering a tool to explore therapeutic strategies targeting aspartyl aminopeptidase in ovarian malignancies.
These polyclonal knockout cells support applications including analysis of aspartyl aminopeptidase in ovarian cancer proliferation and metastasis, investigation of angiotensin signaling within the tumor microenvironment, and screening of peptide-based therapeutics. Compatible assays encompass western blotting, RT-qPCR, angiotensin II-to-III conversion measurements, cell proliferation and apoptosis assays, migration/invasion tests, AT1R signaling analysis, RNA-seq, and xenograft tumor models. The polyclonal nature facilitates robust phenotypic assessment without clonal bias, enabling accurate representation of DNPEP-dependent effects. For further information, please contact Ascent Research.
