The IFI16 Knockout HT29 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population derived from HT29 colorectal adenocarcinoma cells, targeting IFI16 gene disruption. This polyclonal population provides a robust loss-of-function model with heterogeneous knockout events suitable for functional genomics and pathway analysis without clonal bias.
The HT29 cell line was established from a primary colorectal adenocarcinoma of a 44-year-old Caucasian female. These cells display intestinal epithelial properties, including absorptive and secretory functions, and serve as a widely used model for colorectal cancer, epithelial biology, and innate immune signaling studies. Their relevance stems from the ability to investigate tumor-suppressive mechanisms and inflammatory responses in a gut epithelial background.
IFI16 functions as a cytosolic and nuclear DNA sensor that activates innate immunity upon binding double-stranded DNA. It engages STING to trigger TBK1-IRF3-mediated type I interferon production and NF-??B activation, while also nucleating the AIM2 inflammasome complex (ASC/caspase-1) to process IL-1??. As a tumor suppressor, IFI16 stabilizes p53 and induces p21-dependent cell cycle arrest, apoptosis, and senescence. Its expression is induced by interferons, viral DNA, and DNA damage, and it operates through interactions with STING, AIM2, caspase-1, p53, BRCA1, H2AX, and p300/CBP.
Within the HT29 colorectal cancer model, IFI16 knockout provides insights into the intersection of DNA sensing and tumor suppression. HT29 cells retain wild-type p53, enabling study of IFI16-dependent p53 stabilization and downstream effects on cell fate. Loss of IFI16 may attenuate DNA damage checkpoints, reduce senescence, and alter inflammatory cytokine secretion, mimicking features of immune evasion and tumor progression. This model is thus well-suited for dissecting how IFI16 coordinates innate immune activation with genomic integrity in intestinal epithelial tumorigenesis.
Applications include mechanistic studies of STING and AIM2 inflammasome signaling using DNA agonists (poly(dA:dT), cGAMP), analysis of interferon and NF-??B transcriptional responses, and evaluation of p53/p21-mediated tumor-suppressive programs. The knockout cells support Western blotting, RT-qPCR, immunofluorescence, caspase-1 activity assays, cell viability/apoptosis (Annexin V), colony formation, and senescence-associated ??-galactosidase staining. For additional details or to inquire about this product, please contact Ascent Research.
