The IFI27 Knockout 143B Polyclonal Cells represent a CRISPR/Cas9-edited polyclonal knockout cell population derived from the 143B human osteosarcoma cell line. This product comprises a heterogeneous pool of cells carrying targeted disruptions in the IFI27 gene, resulting in a functional loss-of-function model for studying IFI27 biology. The polyclonal format provides a diverse set of genotypes that collectively abrogate gene function, suitable for population-level analyses of gene knockout effects in a physiologically relevant tumor model.
The parental 143B cell line is a well-characterized model of human osteosarcoma, originating from a bone tumor and widely employed to study tumorigenesis, metastasis, and cancer cell signaling. 143B cells exhibit highly tumorigenic and metastatic properties, making them particularly relevant for investigating aggressive bone cancer phenotypes. Their rapid proliferation, invasive capacity, and well-defined genetic background provide a robust platform for assessing gene function in the context of osteosarcoma pathogenesis.
IFI27 is an interferon-stimulated gene that mediates innate antiviral responses and promotes apoptosis by modulating mitochondrial membrane permeability through interactions with BCL2 family members, including BAX and BAK. Upstream signaling involves type I interferons (IFN-??/??) binding to IFNAR1/2 receptors, activating JAK1/TYK2 kinases, and leading to STAT1/STAT2/IRF9 complex formation that drives IFI27 transcription. The IFI27 protein localizes to mitochondria and, upon activation, facilitates cytochrome c release and caspase-3 (CASP3) cleavage. IFI27 also regulates cell cycle progression via p21 (CDKN1A). Consequently, its loss impairs interferon-induced apoptosis and can dysregulate cell proliferation and stress responses.
In 143B cells, this knockout model enables the study of IFI27’s tumor-suppressive functions in osteosarcoma, a cancer often exhibiting aberrant interferon and apoptotic signaling. The highly metastatic nature of the line, combined with IFI27 deficiency, allows examination of how innate immune defects promote tumor progression and metastasis. Researchers can investigate interactions between interferon pathways, mitochondrial apoptosis, and p53 signaling, assessing effects on cell survival, migration, and response to chemotherapeutics or viral challenges.
This knockout product is suitable for a wide range of experimental applications, including interrogation of interferon-??/?? signaling, analysis of antiviral innate immune responses, and assessment of apoptosis using techniques such as western blotting for IFI27, BAX, and BCL2, caspase activity assays, and flow cytometry with Annexin V staining. The 143B background supports viral infection studies (e.g., with VSV-GFP) and drug screening for osteosarcoma therapeutics. High-throughput approaches like RNA-seq transcriptomic profiling further enable global gene expression analysis in the absence of IFI27. For detailed product specifications, availability, and technical consultation, please contact Ascent Research.
