The IFI27 Knockout SK-OV-3 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population targeting the human IFI27 gene in the SK-OV-3 host cell line. This product provides a heterogeneous pool of gene-disrupted cells, minimizing clonal selection artifacts and enabling robust loss-of-function analyses. It serves as a valuable tool for investigating interferon-inducible signaling, mitochondrial-mediated apoptosis, and antiviral innate immune responses within an ovarian adenocarcinoma epithelial context.
The SK-OV-3 cell line is a human ovarian adenocarcinoma epithelial model originally established from the ascitic fluid of a 64-year-old female with ovarian serous cystadenocarcinoma. These cells display overexpression of the HER2 (ERBB2) receptor tyrosine kinase, a molecular hallmark linked to aggressive tumor phenotypes and targeted therapeutic approaches. SK-OV-3 is extensively employed in ovarian cancer research to study oncogenic signaling, drug sensitivity, and the interplay between tumor biology and immune pathways.
IFI27 is an interferon-inducible protein that localizes to mitochondria and promotes apoptosis. Type I interferons (IFN-??/??) bind IFNAR1, activating JAK1 and TYK2 kinases, which phosphorylate STAT1 and STAT2. These associate with IRF9 to form the ISGF3 complex and bind ISRE elements, driving IFI27 transcription. The protein then integrates into the mitochondrial outer membrane, interacting with prohibitin complexes to induce permeabilization. This leads to cytochrome c release and caspase activation, regulated by pro-apoptotic BCL-2 members. Thus, IFI27 connects interferon signaling to intrinsic apoptosis, crucial for antiviral and tumor-suppressive effects.
In the HER2-overexpressing SK-OV-3 ovarian cancer background, IFI27 knockout enables precise interrogation of interferon-driven apoptosis in malignant epithelial cells. This model is instrumental for assessing how loss of IFI27 function influences sensitivity to interferon-based immunotherapy, conventional chemotherapeutics, or targeted agents that impinge on mitochondrial integrity. Researchers can also utilize it to explore potential tumor-suppressive roles of IFI27 and to identify compensatory survival pathways activated upon its deletion. Additionally, the knockout cells offer a platform to study antiviral innate immunity in a cancer context, revealing how oncogenic transformations may rewire host defense mechanisms.
Typical applications include interferon treatment and cell viability assays, Annexin V flow cytometry for apoptosis, and mitochondrial membrane potential measurements using probes like TMRE. Molecular validation involves RT-qPCR and Western blotting for IFI27 and cleaved caspases. RNA-sequencing allows transcriptomic analysis of interferon-stimulated genes in the knockout context, supporting biomarker discovery and drug sensitivity studies. The polyclonal nature of the pool enables assessment of response heterogeneity. For more details, contact Ascent Research.
