The APOBEC3C knockout SK-OV-3 polyclonal cells represent a CRISPR/Cas9-edited polyclonal cell population derived from the SK-OV-3 human ovarian adenocarcinoma epithelial cell line. This reagent features targeted disruption of the APOBEC3C gene, creating a loss-of-function model for investigating the cytidine deaminase’s dual roles in innate antiviral immunity and cancer mutagenesis. The polyclonal format captures heterogeneous editing events across the cell population, providing a robust system for functional studies without clonal selection artifacts.
The parental SK-OV-3 cell line was originally established from the ascites of a 64-year-old Caucasian female with ovarian adenocarcinoma and is widely utilized as a model for epithelial ovarian cancer. These cells are tumorigenic in nude mice and express clinically relevant receptors including EGFR and HER2/neu. SK-OV-3 cells exhibit characteristic epithelial morphology and are commonly employed to study tumor cell proliferation, migration, and signaling pathways contributing to ovarian carcinoma progression.
APOBEC3C encodes a cytidine deaminase that restricts retroviruses and retrotransposons by inducing C-to-U mutations in single-stranded DNA during reverse transcription, thereby contributing to cell-intrinsic antiviral immunity. The enzyme is transcriptionally activated by interferon-?? and interferon-?? through the JAK-STAT signaling axis, involving the receptors IFNAR, kinases JAK1 and TYK2, and transcription factors STAT1, STAT2, and IRF9. Upstream regulators such as IRF1 further modulate its expression. APOBEC3C interacts directly with viral factors like HIV-1 Vif, as well as RNA and ssDNA substrates, and functions cooperatively with other APOBEC3 family members. In cancer, its off-target deamination of genomic DNA promotes mutation signatures, including C-to-T transitions in tumor suppressor genes such as TP53, linking its activity to genome instability and tumor evolution.
In the SK-OV-3 ovarian cancer model, APOBEC3C knockout provides a critical platform to dissect the enzyme’s contributions to mutagenesis, DNA damage responses, and innate immune signaling within an oncogenic context. The cell line’s expression of EGFR and HER2/neu enables exploration of crosstalk between growth factor pathways and APOBEC-driven mutation processes. Disrupting APOBEC3C may alter the rate of spontaneous mutations, influence sensitivity to DNA-damaging agents, and modulate interferon-mediated antiviral defenses, making this model valuable for studying the intersection of immunity and oncogenesis in ovarian tumor cells.
This polyclonal knockout product is suitable for a wide range of experimental applications, including analyzing APOBEC3C-mediated mutation signatures via next-generation sequencing, assessing deamination activity with biochemical assays, and evaluating cellular responses to interferons by RT-qPCR or western blotting. The model supports functional genomics studies employing proliferation and migration assays, drug sensitivity screening, and DNA damage readouts such as ??H2AX immunofluorescence. Researchers can further interrogate transcriptomic changes using RNA-seq to uncover pathways affected by APOBEC3C loss. For additional technical information, please contact Ascent Research.
