The IFI27 Knockout HT29 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population derived from the human colorectal adenocarcinoma HT29 line. This product harbors targeted disruption of the IFI27 gene, which encodes an interferon-inducible mitochondrial pro-apoptotic factor. The polyclonal format presents a heterogeneous pool of edited cells, suitable for studying loss-of-function effects in a context that recapitulates tumor cell diversity.
HT29 cells are an epithelial colorectal adenocarcinoma line with established utility in cancer research. They carry mutations in TP53 and APC, among other genes, and are extensively used to investigate colorectal tumor biology, therapeutic resistance, and signal transduction. Their adherent phenotype and well-characterized growth properties facilitate a broad range of molecular and cellular assays, making them an ideal host for interrogating tumor suppressor-like functions of interferon-stimulated genes.
IFI27 is transcriptionally induced by type I interferons (IFN-??/??) through the ISGF3 complex (STAT1, STAT2, IRF9) downstream of IFNAR1/IFNAR2 and JAK1/TYK2 kinases. The protein localizes to mitochondria, interacting with BCL-2 family and TOM complex to promote mitochondrial outer membrane permeabilization, cytochrome c release, and caspase-9/-3 activation. IFI27 is also a p53 target, linking DNA damage to intrinsic apoptosis. Knockout impairs these pro-death signals, blunting interferon- and p53-dependent cell death.
In HT29 cells, IFI27 loss attenuates interferon-mediated apoptosis, potentially mimicking immune evasion and survival advantages in colorectal tumors. Its absence may promote tumor progression and therapy resistance. This polyclonal knockout model allows examination of IFI27 deficiency in a heterogeneous population, reflecting tumor heterogeneity.
Applications include apoptosis assays (Annexin V, JC-1, cytochrome c release), cell viability and colony formation assays, interferon stimulation and JAK-STAT profiling by RT-qPCR and Western blotting, and drug sensitivity screening. The model is suited for colorectal cancer apoptosis research, antiviral innate immunity studies, and p53?Cmitochondria signaling investigations. For further details, contact Ascent Research.
