The IFIT2 Knockout SK-HEP-1 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal cell population featuring targeted disruption of the IFIT2 gene in the human hepatic adenocarcinoma cell line SK-HEP-1. This product is designed for researchers studying antiviral innate immunity, interferon signaling, and tumor cell biology in a liver cancer context. The polyclonal format preserves the heterogeneity of the original pool and enables robust population-level functional analyses without clonal selection biases. The cells are supplied as a mixed population, allowing direct comparison with wild-type counterpart controls.
SK-HEP-1 is a well-characterized human hepatic adenocarcinoma cell line established from the ascitic fluid of a patient with liver adenocarcinoma. Notably, these cells exhibit endothelial-like properties, making them a unique model for liver cancer biology, tumor angiogenesis, and endothelial transdifferentiation. The line is tumorigenic in immunocompromised mice and is widely employed to investigate hepatocellular carcinoma progression, metastasis, and therapeutic responses. Its dual epithelial and endothelial features provide a versatile background for examining how gene disruptions influence both classic cancer hallmarks and vascular mimicry.
IFIT2 (interferon-induced protein with tetratricopeptide repeats 2) is a central effector of type I interferon-mediated innate immunity. Upon interferon stimulation, IFIT2 is transcriptionally activated by the ISGF3 complex (STAT1-STAT2-IRF9) downstream of IFNAR1-JAK1/TYK2 signaling. The protein forms heteromeric complexes with IFIT1 and IFIT3, which bind eIF3c to globally inhibit cap-dependent translation, thereby restricting viral replication. Beyond antiviral functions, IFIT2 regulates apoptosis and cell migration through interactions with Bcl-2 family members and the TBK1 kinase, linking innate immune signaling to cell survival and motility pathways. Key upstream regulators include IFNA, IFNB, IRF3, and IRF7.
In the SK-HEP-1 background, disruption of IFIT2 enables dissection of its dual roles in antiviral defense and tumor biology. This model is particularly valuable for studying how loss of IFIT2 impacts hepatocellular carcinoma cell proliferation, apoptosis, and migration, as well as responsiveness to interferon-based therapies. Given the endothelial-like characteristics of SK-HEP-1 cells, researchers can also explore IFIT2 involvement in angiogenic signaling and the interplay between innate immunity and tumor microenvironment remodeling.
Typical applications include validation of knockout by RT-qPCR and western blotting, functional assays following interferon stimulation, viral infection challenges to assess innate antiviral activity, Annexin V apoptosis assays, and transwell migration studies. The polyclonal population is suitable for co-immunoprecipitation experiments to map IFIT2-containing complexes, global transcriptome profiling by RNA-seq, and phospho-signaling analysis of downstream pathways. For detailed use instructions and technical support, please contact Ascent Research.
