The IFI27 Knockout HGC-27 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal cell population derived from the HGC-27 human gastric carcinoma line, with targeted disruption of the IFI27 gene. This polyclonal knockout model contains a heterogeneous mix of edited alleles, avoiding clonal selection biases and enabling population-level functional studies. The use of CRISPR/Cas9 ensures robust gene perturbation without the need for single-cell cloning, making it suitable for investigating IFI27-dependent signaling in a complex cellular context.
HGC-27 is a poorly differentiated gastric adenocarcinoma cell line established from a lymph node metastasis, representing an aggressive metastatic gastric cancer model. It is widely used to study gastric tumor biology, including proliferation, invasion, and drug resistance. The metastatic origin and genetic background of HGC-27 provide a clinically relevant platform for examining the role of interferon-inducible genes in advanced gastric carcinoma.
IFI27 encodes a mitochondrial interferon-stimulated protein that integrates type I interferon signaling with apoptotic machinery. Upon IFN-??/?? binding to IFNAR1/IFNAR2, JAK1/TYK2 phosphorylate STAT1/STAT2, which together with IRF9 form the ISGF3 complex that transcriptionally activates IFI27, along with IRF7 and ISG15. IFI27 localizes to mitochondria, interacts with BCL2 family members, and modulates membrane permeability, leading to cytochrome c release and activation of caspases CASP3 and CASP7. It also influences NF-??B signaling, linking antiviral and cell death pathways.
In HGC-27 cells, IFI27 knockout helps dissect the gene??s contribution to apoptosis regulation and interferon-mediated survival signals. Considering the metastatic nature of this line, loss of IFI27 may affect mitochondrial integrity and NF-??B activity, altering responses to inflammatory cues and therapeutic agents. This model enables exploration of how interferon-stimulated mitochondrial functions impact gastric adenocarcinoma progression and metastatic fitness.
Key applications include stimulation with type I interferons followed by RT-qPCR for ISG induction (e.g., ISG15), Annexin V apoptosis assays, and cell viability measurements via MTT/CCK?8. Western blotting for IFI27, cleaved caspases, and BCL2 proteins complements functional studies. Transcriptome profiling and flow cytometry for cell cycle further characterize the knockout phenotype. The model is valuable for drug sensitivity screens targeting interferon or apoptotic pathways. For further details or custom applications, contact Ascent Research.
