The APOBEC3A Knockout A2780 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population with disruption of the APOBEC3A gene in the A2780 human ovarian carcinoma epithelial cell line. This model facilitates investigation of APOBEC3A’s cytidine deaminase functions in cancer and innate immunity, allowing researchers to study its impact on DNA mutagenesis and viral restriction. The polyclonal format provides a heterogeneous population reflecting diverse editing outcomes, suitable for population-level studies without clonal selection bias.
The A2780 line, derived from an untreated ovarian carcinoma patient, displays adherent epithelial morphology and is a standard ovarian cancer model. These cells maintain intact interferon signaling and DNA damage responses, rendering them ideal for studying APOBEC3A-mediated mutagenesis, as ovarian cancer genomes often harbor APOBEC mutational signatures. The adherent growth characteristic supports standard culture conditions and assay compatibility.
APOBEC3A is a cytidine deaminase that induces C-to-T mutations in single-stranded DNA, contributing to antiviral defense and cancer evolution. It is strongly induced by type I interferons (IFN-??/??) via JAK-STAT signaling, leading to formation of the STAT1-STAT2-IRF9 transcription complex. Activated APOBEC3A targets genomic DNA, viral genomes, and LINE-1 retrotransposons, generating ??H2AX-marked DNA double-strand breaks. It interacts with RPA, UNG, and APOBEC3B, integrating with DNA replication and repair. Downstream, ATR-CHK1 and p53 pathways are activated, linking APOBEC3A to genomic instability and apoptosis. Regulatory inputs from TNF-?? and NF-??B further position APOBEC3A at the nexus of inflammation and mutagenesis.
In A2780 cells, APOBEC3A knockout allows dissection of its role in ovarian cancer mutagenesis and drug resistance. Ovarian tumors often show APOBEC hyperactivity, and loss of APOBEC3A can reveal its contribution to spontaneous mutation rates, genotoxic sensitivity, and interferon-induced cytotoxicity. This model also helps discriminate between APOBEC3A and APOBEC3B mutagenic activities and their impact on tumor evolution. Furthermore, it aids in evaluating APOBEC3A’s role in modulating antiviral responses within the tumor microenvironment.
Ideal for cancer mutagenesis, innate immunity, and antiviral research, these cells support assays such as Western blotting, RT-qPCR, immunofluorescence for ??H2AX foci, and whole-genome sequencing for mutation signatures. Functional studies include cytidine deaminase activity, apoptosis, viability, and migration assays. This model is particularly valuable for investigating APOBEC-driven drug resistance in ovarian cancer, enabling the study of how mutagenesis influences the emergence of resistant clones under chemotherapeutic selection. For further details, contact Ascent Research.
