The IFI35 Knockout SK-HEP-1 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal population of SK-HEP-1 human hepatic adenocarcinoma cells with targeted disruption of the IFI35 gene. This polyclonal pool is generated by CRISPR/Cas9-mediated gene disruption, producing a heterogeneous loss-of-function model. The pooled format preserves genetic diversity, enabling robust functional studies in a hepatic cancer context. It is suitable for investigating IFI35 roles in interferon signaling, innate immunity, and hepatocellular carcinoma without clonal selection constraints.
SK-HEP-1 cells are a human hepatic adenocarcinoma line with endothelial characteristics, commonly used for hepatocellular carcinoma (HCC) research. They exhibit tumorigenic properties and liver-specific marker expression, making them valuable for studying cancer signaling, drug responses, and host?Cpathogen interactions. Their adherent morphology and rapid growth support diverse experimental manipulations, providing an ideal host for knockout models to probe gene function in HCC.
IFI35 is an interferon-inducible protein that modulates JAK-STAT signaling downstream of IFN-??/?? and IFN-?? receptors. Following receptor engagement, JAK1/TYK2 phosphorylate STAT1/STAT2, which complex with IRF9 to drive ISG transcription via ISRE elements. IFI35 partners with NMI to enhance this transcriptional response, amplifying antiviral immunity. Expression of IFI35 is induced by IRF3 and IRF7 through RIG-I/MDA5 activation. In cancer, IFI35 additionally regulates NF-??B signaling and apoptosis through Bcl-2 family proteins. It also interacts with BATF2 and proteasome subunits, implicating roles in protein homeostasis.
In SK-HEP-1 cells, IFI35 knockout allows dissection of its dual functions in antiviral immunity and HCC biology. Aberrant interferon signaling is prevalent in HCC, often driven by chronic inflammation or viral infection. IFI35 may act as a tumor suppressor or oncogene, regulating proliferation and apoptosis via STAT and NF-??B pathways. Loss of IFI35 in this model permits investigation of interferon-driven gene regulation, cell cycle effects, IFN therapy sensitivity, and viral replication. The polyclonal population reflects heterogeneous tumor responses, aiding studies of therapeutic resistance.
This polyclonal knockout pool enables diverse assays: IFN stimulation with Western blot/RT-qPCR for IFI35 and ISGs; co-IP for IFI35?CNMI/STAT interactions; ISRE luciferase reporter assays; proliferation (MTT, BrdU) and apoptosis (Annexin V) analyses; and viral infection studies (HCV, VSV). RNA-seq captures transcriptome-wide changes. This model supports research into interferon biology, HCC therapeutic targets, and host?Cvirus interactions. For details, contact Ascent Research.
