The IFIT3 Knockout A-549 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population in which the human IFIT3 gene has been disrupted in the A-549 lung adenocarcinoma epithelial cell line. This heterogeneous pool offers a representative genetic background for loss-of-function studies, reducing artifacts from individual clones, and is designed for investigation of interferon-inducible antiviral mechanisms and cancer signaling.
The A-549 cell line, isolated from a lung adenocarcinoma resected from a 58-year-old Caucasian male, displays epithelial morphology and type II pneumocyte features, making it a standard in vitro model for lung adenocarcinoma. These cells exhibit robust interferon responsiveness and permissiveness to respiratory viruses, including influenza and hepatitis C, supporting their use in both oncology and virology applications.
IFIT3 encodes a tetratricopeptide repeat protein critical for antiviral defense. Upon type I (IFN-??/??) or type II (IFN-??) stimulation, IFIT3 is transcriptionally induced via the JAK-STAT pathway through STAT1/STAT2/IRF9 assembly on ISRE promoters, and its expression is also amplified by IRF3 and IRF7 downstream of RIG-I-like receptors. IFIT3 binds viral RNAs and proteins, inhibiting replication, and forms complexes with IFIT1, IFIT2, IFIT5, and the eIF3 initiation factor to modulate RNA degradation and translation. Additionally, IFIT3 influences apoptosis and cell proliferation, integrating interferon signals with NF-??B-mediated survival pathways.
In the A-549 adenocarcinoma background, IFIT3 knockout allows detailed examination of the gene??s roles at the interface of innate immunity and lung cancer. Loss of IFIT3 is expected to impair viral restriction while potentially altering apoptosis susceptibility and proliferative control, thereby clarifying how interferon-stimulated genes impact tumor cell fitness. This model is instrumental for studies linking antiviral signaling defects to cancer cell adaptation and for testing therapeutic strategies that target interferon pathways in malignancy.
Researchers can employ this knockout model for quantitative analysis of ISG expression by RT-qPCR or RNA-seq after interferon treatment, viral infection assays with influenza virus or hepatitis C virus, and functional apoptosis and cell proliferation readouts using Annexin V/PI staining or MTT assays. Co-immunoprecipitation enables detection of IFIT3 interactions with eIF3 or viral proteins, while Western blotting verifies protein ablation. The cells are also suitable for high-content siRNA or CRISPR screening and drug discovery efforts focused on interferon signaling or viral replication. For further technical information, please contact Ascent Research.
