The IFI27 Knockout AGS Polyclonal Cells provide a CRISPR/Cas9-edited polyclonal knockout population of the IFI27 gene in the AGS human gastric adenocarcinoma epithelial cell line. This product delivers a heterogeneous loss-of-function model that preserves the intrinsic genetic diversity of the parental cells while achieving efficient disruption of the target gene across the cell pool. The polyclonal format is particularly suited for experiments requiring a representative cellular background without clonal artifacts. Researchers can use this tool to interrogate IFI27-mediated signaling pathways in a gastric cancer context with the assurance of robust target-gene ablation.
The AGS host cell line is derived from a gastric adenocarcinoma of a Caucasian patient and represents a widely accepted model for gastric cancer studies. As poorly differentiated gastric epithelial cells, AGS cells retain oncogenic properties such as dysregulated proliferation and apoptosis resistance, making them relevant for exploring tumor biology. This cell line is extensively employed in investigations of gastric carcinogenesis, chemotherapeutic sensitivity, and host-pathogen interactions, offering a clinically meaningful platform for functional genomics.
IFI27 is an interferon-inducible protein residing in mitochondria and the ER that promotes apoptosis through mitochondrial permeabilization. Type I interferons (IFN-??/??) induce IFI27 via the JAK-STAT pathway: binding to IFNAR1/IFNAR2 activates JAK1 and TYK2, phosphorylating STAT1 and STAT2, which together with IRF9 bind ISRE elements. IRF1 and IRF3 also regulate IFI27 transcription. IFI27 interacts with BCL2 family members BAX and BCL2 at mitochondria, triggering cytochrome c release and activation of caspase-9 and caspase-3.
In the context of gastric adenocarcinoma, disruption of IFI27 in AGS cells permits the precise dissection of interferon-stimulated apoptotic pathways that may influence tumor cell survival and immune surveillance. This isogenic model enables researchers to assess the specific contribution of IFI27 to mitochondrial permeabilization and caspase activation in response to interferon, independently of other interferon-induced genes. It is particularly valuable for evaluating how IFI27-dependent apoptosis intersects with gastric cancer progression, viral defense mechanisms, and autoimmune processes, and for testing therapeutic strategies that modulate interferon signaling.
These IFI27 knockout cells are amenable to a wide range of assays, including quantitative real-time PCR (RT-qPCR) to verify transcript loss, Western blotting to confirm protein depletion, Annexin V and caspase-3/9 activity assays to measure apoptosis, immunofluorescence to visualize mitochondrial changes, and flow cytometry for cell viability and cell cycle analysis. They support research applications in gastric cancer cell biology, high-throughput screening of anti-cancer agents, interferon response profiling, and studies of innate immune regulation. For technical specifications or additional information, please reach out to Ascent Research.
