The IFI27 Knockout LoVo Polyclonal Cells are a targeted CRISPR/Cas9-edited polyclonal knockout cell population designed for loss-of-function studies of the human IFI27 gene. This product is generated from the LoVo colorectal adenocarcinoma epithelial cell line and provides a heterogeneous pool of edited cells with disrupted IFI27 expression. The polyclonal format retains genetic diversity, reducing the risk of clonal artifacts and enabling robust functional analyses. This model is well-suited for investigating interferon-induced pathways and apoptosis regulation in a colorectal cancer background.
The LoVo cell line is a well-established human colorectal adenocarcinoma model characterized by mutant APC and KRAS alleles, which drive aberrant Wnt and MAPK signaling, respectively. As an epithelial cell line derived from a metastatic colon cancer lesion, LoVo cells retain key features of colorectal tumor biology, including dysregulated proliferation and altered apoptotic thresholds. This host background provides a relevant context for examining IFI27-dependent processes in cancer cells with compromised tumor suppressor and oncogene signaling.
IFI27 is an interferon-stimulated gene that encodes a mitochondrial-localized protein promoting intrinsic apoptosis. The gene is transcriptionally upregulated by type I interferons (IFN-??/??) via the JAK1/TYK2-STAT1/STAT2-IRF9 signaling cascade and is further regulated by IRF3 and IRF7. At the mitochondria, IFI27 interacts with BAX and the adenine nucleotide translocator, and functionally antagonizes BCL2, leading to mitochondrial outer membrane permeabilization, cytochrome c release, and subsequent activation of caspase-9 and caspase-3. Additionally, IFI27 signaling modulates NF-??B activity, linking apoptosis to inflammatory responses.
In the LoVo colorectal cancer model, IFI27 knockout disrupts interferon-induced cell death and innate antiviral immunity, creating a valuable tool for dissecting tumor cell responses to inflammatory stimuli. Given the prevalence of KRAS and APC mutations in colorectal cancers, this model allows researchers to explore how oncogenic signaling intersects with IFI27-mediated apoptosis. The loss of IFI27 may confer resistance to death receptor and mitochondrial apoptosis pathways, potentially informing mechanisms of immune evasion and treatment resistance in colorectal tumors.
This knockout cell population is applicable to a variety of experimental workflows, including interferon stimulation assays, viral infection studies, and drug sensitivity testing. Researchers can monitor apoptosis by flow cytometry, assess mitochondrial membrane potential, quantify gene expression changes via RT-qPCR and western blotting, and perform global transcriptional profiling with RNA-seq. These assays enable detailed characterization of IFI27??s role in antiviral innate immunity and cancer cell fate decisions. For further technical information, please contact Ascent Research.
