The APOBEC3C Knockout KYSE-150 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population derived from the human esophageal squamous cell carcinoma cell line KYSE-150. This product features a targeted disruption of the APOBEC3C gene, resulting in a loss-of-function model for studying the role of this cytidine deaminase in innate immunity and cancer biology.
KYSE-150 cells originate from an esophageal squamous cell carcinoma (ESCC) of a 49-year-old Japanese female prior to therapy, and are characterized as a poorly differentiated, epithelial cell line. This cell line is widely employed as a model system for ESCC research, including investigations into tumor biology, drug response, and genomic instability.
APOBEC3C encodes a cytidine deaminase that catalyzes C-to-U editing in single-stranded DNA, playing a critical role in innate antiviral defense by hypermutating viral genomes and restricting retrotransposons. Its expression is robustly induced by interferon-alpha and interferon-gamma through the JAK-STAT signaling cascade, involving upstream regulators STAT1, STAT2, and IRF1, as well as the ISGF3 complex (STAT1-STAT2-IRF9). Downstream of cytosolic nucleic acid sensing, APOBEC3C can be activated via the RIG-I/MAVS/TBK1/IRF3 axis. The enzyme interacts with viral capsid proteins and is antagonized by HIV-1 Vif, while its uracil-containing DNA products recruit DNA repair factors such as UNG2 and APE1, linking innate immunity to DNA damage response pathways.
In the context of esophageal squamous cell carcinoma, APOBEC3C-mediated mutagenesis is increasingly recognized as a source of genomic instability, contributing to the accumulation of C-to-T mutations and mutational signatures observed in ESCC genomes. The APOBEC3C Knockout KYSE-150 Polyclonal Cells provide a powerful tool to dissect the contribution of APOBEC3C to the mutational landscape and to evaluate its impact on tumor cell fitness, DNA damage responses, and sensitivity to chemotherapeutic agents such as cisplatin and 5-fluorouracil.
These polyclonal knockout cells are ideally suited for a wide range of investigations, including the validation of APOBEC3C protein depletion by western blotting and mRNA knockdown by RT-qPCR, as well as functional studies of viral restriction using HIV-1 infectivity assays. Researchers can employ whole genome sequencing to analyze mutation signatures and interrogate APOBEC3C-dependent mutational processes. Additionally, these cells enable drug sensitivity profiling with agents like cisplatin and 5-fluorouracil, providing insights into APOBEC3C-mediated chemoresistance. Immunofluorescence can be used to assess APOBEC3C subcellular localization and its absence. For further technical details and ordering information, please contact Ascent Research.
