The IFI27 Knockout KYSE-150 Polyclonal Cells product is a polyclonal population of KYSE-150 esophageal squamous cell carcinoma cells engineered using CRISPR/Cas9-mediated gene disruption to abrogate IFI27 expression. This knockout model provides a loss-of-function system for studying IFI27-dependent processes within a human esophageal cancer background. The polyclonal nature retains potential clonal diversity while targeting the IFI27 locus, making it suitable for pooled functional screens and bulk cellular assays.
The parental KYSE-150 cell line is derived from a human esophageal squamous cell carcinoma and harbors a TP53 mutation, reflecting a commonly altered tumor suppressor gene in this cancer type. These cells exhibit epithelial morphology and are widely utilized as a model system for investigating esophageal cancer biology, including invasion, proliferation, and therapeutic responses. The KYSE-150 line??s genetic background and in vitro growth characteristics make it a relevant host for interrogating interferon-induced apoptosis pathways.
IFI27 is an interferon-inducible protein that localizes to mitochondria and promotes apoptosis by mediating mitochondrial outer membrane permeabilization. Its expression is driven by type I interferons (IFN-?? and IFN-??) through the JAK-STAT cascade, involving receptors IFNAR1/IFNAR2, kinases JAK1 and TYK2, and transcription factors STAT1, STAT2, and IRF9. Downstream, IFI27 interacts with BCL2 family members and mitochondrial proteins to trigger caspase cascades, ultimately executing cell death. Disruption of IFI27 abrogates this pro-apoptotic signal, providing a tool to dissect interferon-regulated intrinsic apoptosis pathways.
In KYSE-150 cells, which carry a TP53 mutation and may be resistant to certain apoptotic stimuli, IFI27 knockout is expected to impair type I interferon-induced cell death and enhance survival. This model enables investigation of how interferon signaling interfaces with mitochondrial apoptosis in esophageal cancer, potentially revealing mechanisms of drug resistance or immune evasion. By comparing knockout and wild-type cells, researchers can evaluate the contribution of IFI27 to interferon-mediated tumor suppression or assess compensatory survival signals.
Typical applications include probing the interferon response in esophageal cancer using western blotting for IFI27 and cleaved caspase-3, RT-qPCR for ISG expression, and flow cytometry for apoptosis (Annexin V/PI). Cell viability assays (MTT/ATP) can quantify survival differences under interferon treatment, while RNA-seq after interferon stimulation reveals global transcriptional changes dependent on IFI27. This polyclonal knockout population is also suited for antiviral pathway studies and drug resistance screens. For further details or technical support, please contact Ascent Research.
