The AGGF1 Knockout UM-UC-3 Polyclonal Cells comprise a CRISPR/Cas9-edited polyclonal knockout cell population derived from the human bladder carcinoma cell line UM-UC-3. This genetically heterogeneous pool of cells harbors targeted disruptions in the AGGF1 locus, established through CRISPR/Cas9-mediated gene editing. Unlike monoclonal knockout lines, this polyclonal population mitigates clonal selection artifacts and provides a robust, unbiased model for studying AGGF1 loss-of-function.
UM-UC-3 is a well-characterized epithelial cell line established from a male patient with transitional cell carcinoma of the bladder. It serves as an in vitro model for high-grade urothelial carcinoma, retaining key molecular features of muscle-invasive disease and broad utility in tumor biology and drug response research.
AGGF1 encodes an angiogenic factor that promotes endothelial cell proliferation and angiogenesis. Its expression is upregulated by hypoxia-inducible factor 1?? (HIF-1??) and further modulated by VEGF and FGF2. AGGF1 functions through homodimerization and interactions with FHA domain-binding proteins and G-patch domain interactors, transducing signals to downstream effectors including PI3K, AKT, ERK1/2, and Cyclin D1, ultimately enhancing VEGF transcription. In these knockout cells, disruption of AGGF1 abolishes its angiogenic function, leading to attenuated PI3K-AKT and ERK pathway activation, reduced VEGF production, and impaired endothelial cell responsiveness.
In bladder cancer, AGGF1 is implicated in tumor angiogenesis and progression. This knockout model enables dissection of AGGF1??s role in urothelial carcinoma-associated angiogenesis and assessment of malignant phenotype dependency on AGGF1-driven signaling. Given the association of AGGF1 mutations with Klippel-Trenaunay syndrome and vascular malformations, the cells also provide a relevant platform for exploring the molecular pathology of vascular disorders.
These polyclonal AGGF1 knockout cells are applicable in angiogenesis research, tumor microenvironment studies, and anti-angiogenic drug screening. Standard assays such as Western blotting and RT-qPCR can verify loss of AGGF1 and downstream targets like VEGF and Cyclin D1. Functional assessments include cell proliferation, endothelial tube formation, migration assays, and VEGF ELISA quantification. This model thus facilitates detailed interrogation of AGGF1-dependent pathways in bladder cancer biology and the development of vascular-targeted therapies. For further information, contact Ascent Research.
