The IFI27 Knockout 786-O Polyclonal Cells represent a CRISPR/Cas9-mediated polyclonal knockout population derived from the 786-O human renal cell carcinoma line, engineered for targeted disruption of the IFI27 gene. This mixed population model avoids clonal selection artifacts and provides a genetically diverse pool for studying gene function. The polyclonal format is supplied as a heterogeneous assortment of edited cells, allowing robust investigation of IFI27-dependent phenotypes in a relevant cancer background.
The 786-O cell line is a widely utilized model of clear cell renal cell carcinoma (ccRCC) derived from a primary tumor of a male patient. These adherent epithelial cells are characterized by a VHL frameshift mutation, leading to constitutive stabilization of hypoxia-inducible factors and loss of pVHL tumor suppressor activity. Additionally, the line is PTEN-deficient, further deregulating PI3K/AKT signaling. This genetic context makes 786-O cells an ideal platform for studying hypoxia-driven tumorigenesis, metabolic reprogramming, and therapeutic resistance.
IFI27 encodes an interferon-inducible mitochondrial protein involved in apoptosis and innate immunity. Transcription is primarily controlled by type I interferon signaling through the IFNAR1/JAK1/STAT1/STAT2/IRF9 pathway, with additional regulation by IRF1, IRF3, and NF-??B. The IFI27 protein localizes to mitochondria, where it interacts with Bcl-2 family members BAX and BAK to compromise membrane integrity, facilitating cytochrome c release and downstream caspase-3/7 activation. It also engages with MAVS, RIG-I, and cGAS-STING pathway components to modulate antiviral responses, and associates with HSP60 and ISGylation machinery, linking it to the unfolded protein response and protein modification networks.
Within the 786-O background, IFI27 knockout enables dissection of interferon-dependent apoptotic pathways in the context of VHL-null ccRCC. Because these cells exhibit aberrant hypoxia signaling and apoptotic thresholds, loss of IFI27 can reveal its contribution to mitochondrial cell death and immune recognition. This model is particularly relevant for exploring how IFI27 influences sensitivity to interferon-based therapies, tyrosine kinase inhibitors like sunitinib, and emerging immunotherapies. Researchers can also study the interplay between IFI27-mediated apoptosis and the tumor microenvironment.
Typical applications include confirmation of IFI27 disruption via western blotting and RT-qPCR, apoptosis assessment by Annexin V/PI flow cytometry, measurement of caspase-3/7 enzymatic activity, and evaluation of mitochondrial membrane potential using JC-1 dye. Further uses encompass RNA-seq transcriptome profiling, drug sensitivity and clonogenic survival assays, and interferon stimulation studies to elucidate antiviral mechanisms. This polyclonal knockout product thus serves as a versatile tool for investigating innate immunity, cell death, and renal cancer biology. For additional details or technical support, please contact Ascent Research.
