The APOBEC3A Knockout KYSE-150 Polyclonal Cells constitute a CRISPR/Cas9-edited polyclonal knockout cell population with targeted disruption of the APOBEC3A gene in the KYSE-150 human esophageal squamous cell carcinoma line. This loss-of-function model enables dissection of APOBEC3A??s roles in innate immunity and cancer-associated mutagenesis. The heterogeneous polyclonal format is useful for studies not requiring clonal purity.
The KYSE-150 host cell line was established from a poorly differentiated esophageal squamous cell carcinoma resected from a Japanese male patient. These cells are widely used as a model for esophageal cancer research due to their malignant properties and genetic background, exhibiting chromosomal instability and aberrant signaling typical of this malignancy. This provides a disease-relevant context for investigating APOBEC3A function.
APOBEC3A is an interferon-inducible cytidine deaminase that edits single-stranded DNA, contributing to antiviral defense and cancer mutagenesis. Its transcription is potently activated by IFN-??, IFN-??, and TNF-?? via upstream regulators IRF3, IRF7, and NF-??B. APOBEC3A interacts with UNG, RPA, and Staufen1, and its catalytic activity drives C-to-T transition mutations and LINE-1 retrotransposon suppression. Downstream, APOBEC3A-induced lesions engage the DNA damage response through ATR and Chk1, promoting clustered mutations (kataegis) and genomic instability.
In esophageal squamous cell carcinoma, APOBEC3A overexpression is associated with a hypermutator phenotype and therapy resistance. In KYSE-150 cells, endogenous APOBEC3A activity fuels tumor evolution through persistent mutagenesis. Disrupting APOBEC3A in this line allows separation of editing-dependent and editing-independent effects, enabling precise examination of mutation burden, retrotransposon mobility, and DNA damage signaling in a relevant genetic background.
These polyclonal knockout cells support diverse functional assays, including C-to-U editing assays, whole-genome mutation signature analysis, RNA-seq transcriptome profiling, western blotting, RT-qPCR of interferon-induced genes, ??H2AX immunofluorescence for DNA damage quantification, clonogenic survival assays following genotoxic treatment, and flow cytometry for cell cycle analysis. Applications span investigation of APOBEC3A-mediated mutagenesis, innate immune signaling, and drug sensitivity in esophageal cancer. For further technical details or ordering information, please contact Ascent Research.
