The IFIT3 Knockout SK-HEP-1 Polyclonal Cells product comprises a CRISPR/Cas9-edited polyclonal knockout cell population derived from the human SK-HEP-1 liver adenocarcinoma cell line, featuring targeted disruption of the IFIT3 gene. This polyclonal format preserves the inherent genetic heterogeneity of the engineered pool while enabling robust loss-of-function studies of IFIT3 in a liver cancer context. The gene-edited pool is designed to serve as a genetically defined model for investigating interferon-stimulated gene function, antiviral innate immunity, and hepatocellular carcinoma biology.
SK-HEP-1 is a well-characterized human liver adenocarcinoma cell line originally isolated from the ascitic fluid of a patient with advanced hepatocellular carcinoma. This adherent cell line is widely employed as an in vitro model for studying hepatic tumor biology, metastatic behavior, drug responses, and interplay with innate immune pathways. Its hepatic origin and metastatic background make it particularly suitable for evaluating gene functions related to cell proliferation, migration, and antiviral signaling within a liver-relevant microenvironment.
IFIT3 (Interferon-Induced Protein with Tetratricopeptide Repeats 3) functions as a critical effector downstream of type I and type III interferon signaling, transcriptionally induced by STAT1/STAT2/IRF9 complexes following activation of IFNAR1/2 by IFN-??/??. IFIT3 forms multiprotein complexes with IFIT1 and IFIT2 and is known to physically interact with TBK1 and STING, bridging innate immune signaling from cytoplasmic RNA sensors such as RIG-I and MDA5 to antiviral transcriptional programs. Mechanistically, IFIT3 contributes to the host antiviral state by promoting the expression of interferon-stimulated genes (ISGs) like OAS1 and MX1, while also modulating cell proliferation and migration through interactions with the STING-TBK1 axis and potential crosstalk with MAVS-dependent pathways.
Disruption of IFIT3 in SK-HEP-1 cells generates a valuable model for dissecting the dual roles of interferon signaling in hepatocellular carcinoma, where chronic inflammation and antiviral defenses are often dysregulated. The IFIT3 knockout background enables examination of how ablation of a key ISG alters the balance between antiviral immunity and pro-tumorigenic processes, including cell migration, invasion, and proliferation. Given that IFIT3 interacts with TBK1 and STING, this model is particularly suited for exploring innate immune checkpoint mechanisms in liver cancer and for profiling the consequences of impaired STING-TBK1 signaling on tumor cell autonomous and non-cell-autonomous behaviors.
This product is suited for a range of experimental applications, including functional characterization of the IFIT3 interactome via co-immunoprecipitation with TBK1, STING, IFIT1, or IFIT2; gene expression analysis by RT-qPCR and Western blotting after IFN treatment; viral infection assays to assess antiviral susceptibility; and phenotypic assays measuring cell migration, invasion, and proliferation in hepatocellular carcinoma. Additionally, the knockout pool supports drug screening targeting JAK-STAT or RIG-I-like receptor pathways and luciferase reporter assays for ISRE or NF-??B activity. For further technical information, please contact Ascent Research.
