The IFI27 Knockout CAL-27 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population generated from the CAL-27 human tongue squamous cell carcinoma line. This product comprises a heterogeneous pool of cells with targeted disruption of the IFI27 gene, enabling loss-of-function analysis in an epithelial cancer context. The polyclonal format captures diverse editing events without clonal selection, offering a suitable tool for experiments where population-level gene inactivation suffices to probe the roles of IFI27 in oncogenic and innate immune pathways.
CAL-27 is an epithelial cell line derived from a 56-year-old male with tongue squamous cell carcinoma. It exhibits aggressive features of head and neck cancer, including dysregulated apoptosis and inflammatory signaling. Widely used in oral cancer research, CAL-27 enables studies of tumor cell proliferation, migration, invasion, and drug sensitivity. Introducing IFI27 knockout into this model provides a tractable system for dissecting interferon responses in a malignancy-relevant setting.
IFI27 encodes an interferon-inducible protein that promotes apoptosis and antiviral innate immunity. Its transcription is activated by type I interferons (IFN-??/??) via the JAK-STAT pathway, requiring phosphorylation of STAT1 and STAT2, assembly with IRF9 into the ISGF3 complex, and binding to the IFI27 promoter. Expressed IFI27 localizes to mitochondria, inducing membrane permeabilization, cytochrome c release, and activation of caspases-3 and -7. It interacts with Bcl-2 family members to tip the balance toward apoptosis. Additionally, IFI27 modulates NF-??B signaling, linking interferon responses to inflammatory and survival pathways, thus integrating antiviral immunity with cell fate decisions.
In CAL-27 oral squamous cell carcinoma, IFI27 knockout is expected to reduce apoptotic sensitivity to interferon stimulation and may alter NF-??B transcriptional programs. Given that head and neck cancers often resist apoptosis and evade immunity, this polyclonal knockout model helps assess IFI27??s role in tumor survival, proliferation, and response to interferon-based therapies. Disruption of this gene can reveal imbalances in cell death and survival signaling, shedding light on tumor immune manipulation. The polyclonal nature also reflects genetic heterogeneity, enhancing translational relevance.
These IFI27 knockout cells are amenable to functional assays such as annexin V apoptosis assays and caspase-3/-7 activity measurements. qRT-PCR and Western blotting can confirm gene disruption and assess compensatory interferon-stimulated gene changes. MTT proliferation assays and Transwell migration/invasion assays evaluate tumorigenic properties. Drug response screening can explore the impact of IFI27 loss on chemosensitivity or interferon-inducing agents. This makes the IFI27 Knockout CAL-27 Polyclonal Cells a versatile tool for oral cancer apoptosis, innate immunity, and preclinical drug evaluation. For inquiries, contact Ascent Research.
