The APOBEC3C Knockout MCF-7 Polyclonal Cells product provides a CRISPR/Cas9-edited polyclonal knockout cell population in which the APOBEC3C gene has been disrupted. This gene-editing strategy enables loss-of-function studies of APOBEC3C in a heterogeneous pool of MCF-7 cells, modeling natural genetic variation without clonal selection. The polyclonal format preserves the inherent cellular diversity of the edited population, offering a robust experimental system for studying APOBEC3C-dependent processes while mitigating clone-specific artifacts.
These knockout cells are derived from the MCF-7 human breast adenocarcinoma cell line, which is characterized by its epithelial origin and expression of estrogen receptor (ER) and progesterone receptor (PR) while lacking HER2 amplification (ER+, PR+, HER2?). MCF-7 is a widely employed model in breast cancer research, particularly for hormone-responsive tumors. Its well-documented genomic landscape and extensive characterization make it an ideal host for dissecting gene function in mammary epithelial biology and oncogenesis.
APOBEC3C encodes a cytidine deaminase that catalyzes C-to-U deamination in single-stranded DNA, functioning as an antiviral restriction factor against retroviruses such as HIV-1 and hepadnaviruses. Its expression is strongly induced by type I interferons (IFN-?? and IFN-??) through the JAK-STAT pathway. Upon IFN binding to IFNAR1/IFNAR2 receptors, downstream kinases JAK1 and TYK2 phosphorylate STAT1 and STAT2, which complex with IRF9 to form ISGF3, thereby transcriptionally activating APOBEC3C. The enzyme interacts with APOBEC3G, HIV-1 Vif, UNG, MOV10, and AGO2, and its activity targets viral genomes and host genomic DNA, leading to hypermutation and DNA damage responses.
In the MCF-7 breast cancer context, APOBEC3C-mediated deamination may contribute to subclonal mutagenesis and tumor evolution. Aberrant APOBEC activity has been implicated in cancer genomic instability, and the interplay between interferon signaling and APOBEC3C expression can influence tumor cell fitness and response to immune pressures. This knockout model enables precise dissection of APOBEC3C??s mutagenic contributions versus its antiviral roles in an ER+ breast cancer background, facilitating studies on how innate immune pathways shape breast adenocarcinoma progression and therapy resistance.
Researchers can employ these polyclonal knockout cells to investigate antiviral innate immunity through HIV-1 restriction assays, mutation detection by differential DNA denaturation PCR (3D-PCR), and deaminase activity measurements. The model also supports analysis of interferon-responsive gene networks via RT-qPCR, RNA-seq, and western blotting, and enables immunofluorescence-based localization studies. It further facilitates DNA damage response assessments and cancer mutagenesis research. By combining the MCF-7 lineage with APOBEC3C disruption, this tool provides a powerful platform for advancing understanding of APOBEC biology in infectious disease and oncology. For further details, please contact Ascent Research.
