The DPP9 Knockout A2780 Polyclonal Cells provide a CRISPR/Cas9-edited polyclonal population with disrupted DPP9 in the A2780 ovarian carcinoma line. This genetically mixed knockout pool eliminates DPP9 protease activity, offering a versatile loss-of-function model without single-cell cloning, suitable for functional studies.
The A2780 cell line, established from an untreated endometrioid ovarian adenocarcinoma, is a standard epithelial ovarian cancer model. It retains tumor characteristics and is widely used for oncogenesis, metastasis, and drug response studies, particularly with platinum-based agents. Integrating the DPP9 knockout into this background enables investigation of protease-dependent mechanisms in ovarian cancer.
DPP9 is a serine protease that cleaves N-terminal dipeptides, acting as a negative regulator of NLRP1 and CARD8 inflammasomes. Under normal conditions, DPP9 maintains these sensors in an inactive state. Its disruption leads to spontaneous inflammasome assembly, ASC recruitment, and caspase-1 activation, driving pyroptosis. DPP9 also regulates cell adhesion and migration by interacting with fibronectin (FN1) and integrin ??1 (ITGB1). The protease is induced by IFN?? and inflammatory cytokines and forms homodimers, directly binding NLRP1 and CARD8. Thus, DPP9 ablation simultaneously impacts innate immunity and adhesion dynamics.
In A2780 cells, DPP9 knockout triggers inflammasome-mediated pyroptosis and impairs fibronectin-dependent adhesion and migration. This dual phenotype models both inflammatory cell death and metastatic behavior relevant to ovarian cancer. The model is ideal for studying cross-talk between inflammasome activation and tumor cell motility, leveraging the epithelial cancer background to dissect DPP9??s roles in progression and immune evasion.
These cells support inflammasome studies using cleaved caspase-1 western blot, IL-1?? ELISA, and LDH release assays. Adhesion/migration assays evaluate DPP9??s role in tumor dynamics. The model aids DPP9 inhibitor screening with enzymatic activity assays and enables autoinflammatory disease research via NLRP1 puncta immunofluorescence and inflammasome RT-qPCR. It also facilitates apoptosis versus pyroptosis comparisons. Contact Ascent Research for assistance.
