The APOBEC3C Knockout UM-UC-3 Polyclonal Cells product comprises a polyclonal population of UM-UC-3 human bladder urothelial carcinoma cells genetically modified using CRISPR/Cas9 to disrupt the APOBEC3C gene. This polyclonal knockout cell pool provides a stable loss-of-function model for APOBEC3C, eliminating its enzymatic activity without clonal selection. The targeted gene disruption ensures robust abrogation of APOBEC3C expression, enabling detailed functional studies in a relevant bladder cancer background.
UM-UC-3 is an established cell line derived from a male patient with transitional cell carcinoma (urothelial carcinoma) of the bladder. It serves as a widely used model for invasive bladder cancer research, retaining key genetic and phenotypic features of the primary tumor. The cell line’s characteristics, including typical bladder cancer mutations and invasive properties, make it an appropriate host for investigating gene function in the context of urothelial carcinoma.
APOBEC3C functions as a cytidine deaminase that introduces C-to-U mutations in single-stranded DNA, thereby contributing to both innate antiviral defense and cancer mutagenesis. Its expression is transcriptionally regulated by interferon-alpha/beta (IFN-??/??) through the JAK1/TYK2-STAT1-STAT2-IRF9 signaling axis. Once activated, APOBEC3C generates uracil lesions in genomic DNA, which are processed by uracil DNA glycosylase (UNG) and apurinic/apyrimidinic endonuclease 1 (APE1). This processing triggers DNA damage response pathways involving ATM and ATR kinases, leading to phosphorylation of downstream effectors such as H2AX. Persistent APOBEC3C activity can induce C-to-T mutations in critical genes like TP53, driving genomic instability and tumor evolution.
In the UM-UC-3 bladder cancer model, APOBEC3C-mediated mutagenesis is likely a key contributor to the APOBEC-associated mutational signatures prevalent in urothelial carcinomas. Disruption of APOBEC3C in this cell line allows researchers to dissect its role in sustaining mutagenesis, modulating DNA damage responses, and influencing tumor cell behavior. This knockout model is particularly valuable for examining how loss of APOBEC3C alters proliferation, migration, invasion, and sensitivity to chemotherapeutic agents such as cisplatin and gemcitabine, thereby revealing its impact on bladder cancer progression and treatment resistance.
Researchers can employ this polyclonal knockout cell population to investigate APOBEC3C function in bladder cancer mutagenesis and innate immune responses. Representative assays include Western blotting and RT-qPCR for validation of knockout, cell proliferation and migration/invasion assays to assess tumorigenic properties, whole-genome sequencing to characterize mutational signatures, and DNA damage evaluation via ??H2AX foci. Antiviral response assays and drug sensitivity testing with cisplatin or gemcitabine further enable studies on therapeutic resistance. For additional information or to request a quotation, please contact Ascent Research.
