The APOBEC3C Knockout A-549 Polyclonal Cells product comprises a CRISPR/Cas9-edited polyclonal knockout cell population derived from the A-549 cell line, with targeted disruption of the APOBEC3C gene. This gene-edited pool provides a heterogeneous loss-of-function model that bypasses clonal selection biases, enabling robust assessment of APOBEC3C-dependent phenotypes without the confounding effects of monoclonal adaptation. The polyclonal nature ensures representation of diverse genetic backgrounds within the knockout context, making the model suitable for population-level analyses of gene function.
The parental A-549 cell line is a widely employed human lung adenocarcinoma model, established from the carcinoma tissue of a 58-year-old Caucasian male. These adherent epithelial cells are extensively used in respiratory system research, drug metabolism studies, and cancer biology investigations, particularly for dissecting molecular mechanisms of lung tumorigenesis and evaluating therapeutic agents. Their well-characterized growth properties and susceptibility to genetic manipulation render them an optimal host for CRISPR-based gene disruption.
APOBEC3C encodes an interferon-inducible cytidine deaminase that restricts retroviruses by deaminating cytidine to uridine in single-stranded DNA during reverse transcription, inducing G-to-A hypermutations. Interferons (alpha, beta, gamma) upregulate APOBEC3C via STAT1 and IRF3. It interacts with HIV-1 Vif and replication protein A (RPA) and operates within innate immune pathways such as cGAS-STING and JAK-STAT. In tumorigenesis, off-target APOBEC3C activity contributes to kataegis and mutation signatures in lung adenocarcinoma, involving downstream uracil DNA glycosylase (UNG) and cooperation with APOBEC family members A3A, A3B, and A3G.
In A-549 lung adenocarcinoma cells, knocking out APOBEC3C enables dissection of its dual roles in viral restriction and cancer-associated mutagenesis. This model is crucial for studying how interferon-driven APOBEC3C activity balances antiviral responses against off-target DNA damage, and for assessing the contribution of APOBEC-mediated mutagenesis to drug resistance and tumor evolution in non-small cell lung cancer.
This polyclonal knockout product is suitable for a variety of applications, including western blotting and RT-qPCR for knockout validation, lentiviral infectivity assays to measure viral restriction, and DNA cytidine deamination assays to quantify enzymatic activity. Immunofluorescence and flow cytometry enable evaluation of subcellular localization and population-level expression, while RNA-seq captures transcriptomic changes. These cells support advanced research in innate antiviral immunity, APOBEC-induced tumor evolution, cancer mutagenesis, and viral restriction factor studies. For technical inquiries or additional product information, please contact Ascent Research.
