The APOBEC3A Knockout HGC-27 Polyclonal Cells represent a CRISPR/Cas9-edited polyclonal knockout cell population derived from the HGC-27 human gastric adenocarcinoma cell line. This product features targeted disruption of the APOBEC3A gene, which encodes an innate immune cytidine deaminase. The polyclonal format comprises a heterogeneous pool of cells carrying diverse CRISPR-mediated edits, eliminating the need for single-cell cloning and providing a robust loss-of-function model. This knockout model enables researchers to investigate APOBEC3A-dependent processes in a gastric cancer context without the confounds of clonal variation.
HGC-27 is a gastric carcinoma epithelial cell line originally established from the metastatic lymph node of a patient with gastric adenocarcinoma. It serves as a widely used model system for gastric cancer research, retaining key characteristics of gastric epithelial cells. These cells display epithelial morphology and are employed in studies of gastric cancer biology, including proliferation, invasion, and drug response. The HGC-27 background is particularly relevant for examining the role of APOBEC3A in gastric tumorigenesis and innate immune responses within the gastric epithelium.
APOBEC3A functions as a DNA cytidine deaminase that catalyzes C-to-U hypermutation in single-stranded DNA, a process critical to innate immunity and antiviral defense. Its expression is induced by type I interferons (IFN-??/??) through the JAK-STAT signaling axis, involving upstream receptors IFNAR1/IFNAR2, kinases JAK1 and TYK2, and the transcription factor complex STAT1/STAT2/IRF9. APOBEC3A interacts with the RPA complex and single-stranded DNA to execute its editing activity. Downstream consequences include genomic hypermutation, activation of DNA damage checkpoints, cell cycle arrest, and apoptosis, collectively contributing to both antiviral restriction and cancer-associated mutagenesis.
In gastric cancer, APOBEC3A-mediated mutagenesis is implicated in generating tumor mutational burden, driving clonal evolution and therapeutic resistance. Knockout of APOBEC3A in HGC-27 cells eliminates this mutagenic activity, providing a clean genetic background to dissect its role in cancer progression. This model is particularly valuable for assessing how APOBEC3A influences DNA damage repair pathways and genomic instability in gastric epithelial cells. Researchers can directly compare wild-type and knockout populations to evaluate APOBEC3A-dependent changes in mutation signatures, DNA damage responses, and cellular phenotypes relevant to gastric cancer pathology.
This polyclonal knockout cell model supports a wide range of applications, including investigation of APOBEC3A-mediated mutagenesis in gastric cancer, study of innate immune signaling and viral restriction, evaluation of DNA damage repair pathways, and analysis of tumor evolution and heterogeneity. Representative assays include Western blotting and RT-qPCR for confirming APOBEC3A ablation, DNA sequencing for mutation analysis, immunofluorescence for protein localization, flow cytometry for cell cycle and apoptosis, and drug sensitivity screens with genotoxic agents. RNA-seq and ??H2AX ChIP-seq facilitate transcriptomic and DNA damage mapping. For further information or to discuss custom applications, please contact Ascent Research.
