The IFI27 Knockout T-47D Polyclonal Cells represent a CRISPR/Cas9-edited polyclonal knockout population generated from the T-47D human breast ductal carcinoma cell line. This product consists of a heterogeneous pool of cells with targeted disruption of the IFI27 gene, creating a loss-of-function model to study interferon-induced apoptosis and innate immune signaling. The polyclonal nature preserves genetic diversity, minimizing clonal selection artifacts and enabling robust functional assessments in a hormone-responsive breast cancer context.
The T-47D host cell line was established from the pleural effusion of a 54-year-old female with invasive ductal carcinoma. As an epithelial, hormone-responsive breast cancer model, T-47D cells express estrogen receptor (ER), progesterone receptor (PR), and androgen receptor (AR), making them invaluable for researching hormone signaling, endocrine therapy resistance, and tumor biology. This background is particularly relevant for investigating how interferon-stimulated genes influence breast cancer cell fate under immune activation.
IFI27 is an interferon-stimulated gene that encodes a protein promoting apoptosis and inhibiting proliferation through mitochondrial dysfunction. It is transcriptionally induced by type I interferons (IFN-??, IFN-??) via the JAK-STAT pathway: ligand-bound IFNAR1/IFNAR2 receptors activate JAK1 and TYK2 kinases, which phosphorylate STAT1 and STAT2. Phosphorylated STAT1-STAT2 heterodimers recruit IRF9 to form the ISGF3 complex, driving IFI27 expression. The IFI27 protein interacts with Bcl-2 family members and mitochondrial proteins, leading to caspase activation and mitochondrial outer membrane permeabilization, thereby integrating extracellular interferon signals with the intrinsic apoptosis machinery.
In T-47D cells, IFI27 serves as a critical mediator connecting type I interferon signaling to mitochondrial apoptosis. Knockout of IFI27 in this ER+/PR+/AR+ background impairs interferon-induced cell death, providing a model to dissect immune-mediated tumor suppression and the interplay between hormone receptor pathways and innate immunity. Researchers can use this model to explore how IFI27 loss alters sensitivity to interferon-based therapies or modulates tumor cell survival under inflammatory stress, offering insights into breast cancer immune evasion and therapeutic resistance.
This polyclonal knockout cell population supports diverse experimental approaches. It is well-suited for quantifying gene expression by RT-qPCR, detecting proteins via western blotting, and measuring apoptosis with Annexin V or caspase-3/7 assays. Interferon stimulation combined with phospho-STAT1 detection enables monitoring of JAK-STAT activation. Cell viability (MTS), migration assays, and RNA-seq transcriptomics further expand its utility. Key applications include cancer immunotherapy target validation, screening for mitochondrial apoptosis modulators, and dissecting innate immune signaling in breast cancer. For additional information, please contact Ascent Research.
