APOBEC3C Knockout CAL-27 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population derived from the human tongue squamous cell carcinoma cell line CAL-27. This engineered model enables loss-of-function studies of APOBEC3C, a cytidine deaminase involved in innate immunity and restriction of retroviruses and retrotransposons, providing a potent tool for investigating APOBEC-mediated mutagenesis in head and neck cancer.
The CAL-27 parental cell line originates from a human tongue squamous cell carcinoma and is widely used as an epithelial cancer model. CAL-27 cells retain key molecular features of head and neck squamous cell carcinoma (HNSCC) and are commonly employed in studies of tumor biology, invasion, and drug response. Their epithelial origin and genetic background make them particularly suitable for examining the roles of host restriction factors such as APOBEC3C in the context of HNSCC.
APOBEC3C is a member of the AID/APOBEC cytidine deaminase family that catalyzes C-to-U editing on single-stranded DNA and RNA, serving as a critical component of the innate immune defense against retroviral infection and retrotransposon mobilization. Its expression is strongly induced by type I interferons (IFN-??/??) through STAT1 and IRF3 signaling. APOBEC3C interacts with the HIV-1 accessory protein Vif, which counteracts its antiviral activity, and it functions alongside other APOBEC3 family members (APOBEC3G and APOBEC3F) and the cofactor core-binding factor subunit beta (CBFB). In addition to restricting HIV-1 cDNA and retrotransposon RNA, APOBEC3C can deaminate genomic DNA, contributing to mutation signatures observed in multiple cancers.
In CAL-27 cells, APOBEC3C-mediated deaminase activity may contribute to the accumulation of somatic mutations often seen in HNSCC. By disrupting APOBEC3C expression, this polyclonal knockout population allows researchers to dissect its role in driving genomic instability, tumor evolution, and potential resistance to therapy. Moreover, the loss of APOBEC3C may impair the cell’s ability to restrict retroviral replication, enabling studies that separate cancer-autonomous functions from its antiviral activities.
This knockout model is suitable for a range of experimental applications, including western blotting and RT-qPCR for confirmation of gene disruption, viral infectivity assays to assess changes in restriction capacity, DNA deamination assays to quantify editing activity, and functional studies such as cell viability, migration, and invasion assays. It provides a valuable platform for profiling innate immune responses, investigating APOBEC-driven mutagenesis in head and neck cancer, and identifying host factors in viral restriction. For further information and technical support, please contact Ascent Research.
