The DNPEP Knockout A2780 Polyclonal Cells constitute a CRISPR/Cas9-edited polyclonal cell population engineered for targeted disruption of the DNPEP gene in the A2780 human ovarian cancer cell line. This product provides a robust loss-of-function model, generated via CRISPR/Cas9-mediated gene disruption, resulting in a heterogeneous pool of cells with ablated DNPEP expression. As a polyclonal knockout cell population, it avoids clonal artifacts and enables the study of gene function in a mixed genetic background, closely simulating the heterogeneity observed in tumor biology.
The host A2780 cell line is a well-characterized human ovarian endometrioid adenocarcinoma epithelial cell line, widely employed as an in vitro model for ovarian carcinoma research. Originating from an untreated patient, A2780 cells are estrogen-responsive and exhibit robust epithelial morphology, making them suitable for investigating hormone-driven oncogenic processes, drug resistance mechanisms, and signaling pathways relevant to ovarian cancer pathophysiology.
DNPEP encodes a cytosolic aspartyl aminopeptidase that selectively removes N-terminal aspartic and glutamic acid residues from peptide substrates, thereby contributing to intracellular protein turnover and the processing of regulatory peptides. Its activity is regulated upstream by estrogen signaling and cellular stress responses, and it functions downstream of these cues to modulate levels of key effectors such as angiotensin IV and oxytocin. Consequently, DNPEP intersects with the renin-angiotensin system (RAS) and oxytocin signaling pathways, interacting with proteasome components and peptide substrates that include angiotensin IV and oxytocin. Through these interactions, DNPEP influences peptide hormone activation and downstream signaling cascades.
In the context of ovarian cancer, DNPEP loss-of-function in A2780 cells, as achieved in this knockout model, disrupts the normal catabolism of vasoactive and mitogenic peptides, leading to their accumulation. This perturbation can alter cellular proliferation, migration, and apoptotic thresholds, potentially affecting sensitivity to platinum-based chemotherapeutics such as cisplatin. Given that estrogen signaling is a pivotal upstream regulator and that A2780 cells retain estrogen responsiveness, this model is particularly suited for dissecting the convergence of hormonal cues and aminopeptidase activity in ovarian cancer progression and drug response.
Typical research applications include functional characterization of DNPEP via Western blotting and RT-qPCR to confirm gene disruption, quantification of angiotensin IV levels by ELISA, assessment of cell viability through MTT assays, evaluation of motility using wound healing assays, and measurement of cisplatin sensitivity. Additionally, immunofluorescence enables subcellular localization studies of DNPEP and its interacting partners. These applications position the DNPEP Knockout A2780 Polyclonal Cells as a valuable tool for peptidomics and signaling pathway dissection in ovarian cancer research. For further inquiries and technical support, please contact Ascent Research.
