The APOBEC3C Knockout LoVo Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population derived from the LoVo human colorectal adenocarcinoma epithelial line, with disrupted APOBEC3C to create a loss-of-function model. This polyclonal format offers a heterogeneous knockout pool, minimizing clonal artifacts and enabling investigation of APOBEC3C-mediated cytidine deamination in colorectal cancer mutagenesis and innate antiviral immunity.
The LoVo host cell line originates from a metastatic supraclavicular lymph node of a male with left-sided colon adenocarcinoma, carrying mutations in APC, KRAS, and TP53. As an intestinal epithelial model, LoVo is widely applied in colorectal cancer research to study tumor progression, metastasis, and therapy. Its epithelial derivation is particularly suited for examining APOBEC3C function, given the prevalence of APOBEC mutational signatures in colorectal tumors.
APOBEC3C is a single-stranded DNA cytidine deaminase that catalyzes C-to-U deamination, causing C-to-T mutations during replication. Its expression is induced by interferon-alpha and interferon-gamma via IRF3, IRF7, NF-kappaB, and STAT1. It restricts HIV-1 and retrotransposons by mutagenizing cDNA, a process opposed by HIV-1 Vif, and interacts with ssDNA, APOBEC3A, APOBEC3B, and RPA. Off-target deamination of host DNA at TC motifs feeds into base excision repair, where UNG, APE1, and DNA polymerase beta process uracil lesions, linking APOBEC3C activity to genome instability and DNA damage responses.
In the LoVo background, APOBEC3C-driven mutagenesis may accelerate genetic diversity and tumor evolution under APC/KRAS/TP53 mutant selection. Its interplay with APOBEC3A, APOBEC3B, and base excision repair pathways positions this knockout model as essential for dissecting APOBEC3C-specific contributions to mutational signatures and drug resistance, especially given LoVo sensitivity to genotoxic agents.
Applications include Western blot and RT-qPCR for knockout validation; deaminase activity assays via differential DNA denaturation PCR; and immunofluorescence for subcellular localization. HIV-1 infectivity and retrotransposon mobilization assays assess viral restriction, while proliferation and drug sensitivity screens define APOBEC3C??s role in therapy response. This tool supports functional genomics of APOBEC proteins in cancer, innate immunity, and DNA repair. For further information, please contact Ascent Research.
