The IFI27 Knockout KYSE-30 Polyclonal Cells consist of a CRISPR/Cas9-edited population of human KYSE-30 esophageal squamous cell carcinoma (ESCC) cells harboring targeted disruption of the IFI27 gene. Produced without single-cell cloning, this polyclonal knockout pool offers a heterogeneous loss-of-function model that avoids clonal artifacts. The product is designed for investigations of IFI27 function in interferon signaling, apoptosis regulation, and innate immunity within an ESCC context.
KYSE-30 is a well-characterized human ESCC cell line derived from a male patient, widely used as a model for esophageal cancer research. These cells exhibit hallmark malignant properties, including dysregulated proliferation, migration, and drug sensitivity, making them a representative platform for studying oncogenic mechanisms and therapeutic interventions. Introducing an IFI27 knockout in this background enables precise dissection of interferon-inducible pathways in ESCC pathophysiology, offering a clinically relevant setting for evaluating the impact of IFI27 loss.
IFI27 is a mitochondrial protein strongly induced by type I interferons (IFN-??/??) via the JAK-STAT cascade. Interferon binding to IFNAR1/IFNAR2 receptors activates JAK1 and TYK2, leading to phosphorylation of STAT1 and STAT2, which heterodimerize and recruit IRF9 to form the ISGF3 complex, driving IFI27 transcription. Once expressed, IFI27 localizes to mitochondria, where it interacts with key apoptotic regulators such as BAX and BCL2, modulating mitochondrial membrane integrity and cytochrome c (CYCS) release. It also engages with TRAF2, ASK1, and NDUFS4, linking interferon signals to cell death and mitochondrial dynamics. Disruption of IFI27 in this product eliminates these interactions, permitting detailed analysis of its role in apoptosis and antiviral responses.
In ESCC, IFI27 expression is often upregulated, potentially contributing to apoptosis resistance and immune evasion. This knockout model enables researchers to investigate how loss of IFI27 affects ESCC cell survival, interferon sensitivity, and chemotherapeutic responsiveness. By depleting IFI27 in KYSE-30 cells, users can explore the interplay between mitochondrial apoptosis and innate immune pathways in esophageal cancer, identifying vulnerabilities for therapeutic targeting. The model is particularly valuable for studying the crosstalk between Type I interferon signaling and BCL2 family-regulated apoptosis in the context of solid tumors.
Typical applications include analyzing apoptosis by flow cytometry (annexin V/PI) and Western blotting of BAX, BCL2, cleaved CASP3, and cytochrome c; assessing cell viability and drug sensitivity using MTT or luminescent assays; evaluating migration and invasion with transwell systems; and profiling transcriptomic changes via RT-qPCR or RNA-seq after interferon stimulation. The polyclonal IFI27 knockout is also suitable for antiviral response studies and high-throughput screening. For further technical details, please contact Ascent Research.
