The APOBEC3C Knockout Ca Ski Polyclonal Cells are a human CRISPR/Cas9-edited polyclonal knockout cell population targeting the APOBEC3C gene in the Ca Ski cervical cancer cell line. This polyclonal pool was generated using CRISPR/Cas9-mediated gene disruption to ablate APOBEC3C expression, creating a stable loss-of-function model. Unlike monoclonal lines, the polyclonal format preserves population-level heterogeneity, minimizing clonal artifacts while enabling robust bulk analyses such as pooled functional screens and biochemical assays.
The host cell line, Ca Ski, is an adherent epithelial cell model originally derived from a cervical epidermoid carcinoma metastasis. These cells are notable for containing integrated human papillomavirus type 16 (HPV-16) genomic DNA, establishing them as a central system for studying HPV-driven malignancy. Their epithelial nature and HPV-16 positivity make Ca Ski cells particularly relevant for investigating the interplay between viral oncogenesis and host innate defense mechanisms in the context of cervical cancer.
APOBEC3C is a cytidine deaminase that functions as a potent restriction factor against exogenous and endogenous retroelements. It catalyzes the deamination of cytidine to uridine in single-stranded DNA, predominantly targeting reverse transcription intermediates of retroviruses such as HIV-1, thereby introducing lethal C-to-U mutations. APOBEC3C expression is induced by type I interferons (IFN-??/??) via the JAK-STAT signaling cascade, with activation of interferon regulatory factors IRF3 and IRF7, and it can also be regulated by NF-??B. The enzyme physically interacts with the HIV-1 accessory protein Vif, which counteracts its antiviral activity, and cooperates with other APOBEC3 family members to restrict retrotransposon mobilization.
In the HPV-positive Ca Ski background, disruption of APOBEC3C offers a unique platform to decipher the contributions of innate antiviral immunity to cervical cancer progression. HPV persistence and integration are influenced by host defense mechanisms, and APOBEC3C-mediated editing may modulate viral genome stability and retrotransposon activity. This knockout model therefore enables investigation of how loss of a key restriction factor impacts HPV-host interactions, mutagenic processes, and the development of cervical carcinoma.
This polyclonal knockout cell pool is well-suited for diverse experimental applications, including western blotting, RT-qPCR, DNA deamination assays, viral infectivity studies, retrotransposon mobilization assays, and immunofluorescence. Researchers can use it to dissect APOBEC3C??s role in HIV-1 restriction, APOBEC3 family functions, HPV-related immunobiology, and cancer-associated mutagenesis. For further product information, please contact Ascent Research.
