BST2 Knockout HT29 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population derived from the HT29 human colorectal adenocarcinoma cell line. This product features targeted disruption of the BST2 gene, resulting in a loss-of-function model suitable for investigating the biological roles of BST2 (tetherin) in innate immunity, inflammation, and cancer biology. The polyclonal format provides a heterogeneous pool of edited cells useful for functional studies without clonal isolation.
The HT29 cell line originates from a primary colon adenocarcinoma of a 44-year-old female and is widely employed as an in vitro model for colorectal cancer and intestinal epithelial cell biology. These cells retain key characteristics of colonic epithelium, including the ability to polarize and form tight junctions, and are extensively used in studies of signal transduction, drug metabolism, and host-pathogen interactions.
BST2 encodes tetherin, an interferon-inducible restriction factor that inhibits viral egress by physically tethering budding virions to the plasma membrane. Beyond its antiviral function, BST2 activates NF-??B signaling, promoting transcription of pro-inflammatory cytokines such as IL-6 and TNF-??, and also modulates cell adhesion and migration. Its expression is induced by type I interferons via JAK-STAT signaling and interferon regulatory factors, and it is counteracted by viral proteins like HIV-1 Vpu. Mechanistically, BST2 interacts with components of the ESCRT machinery, including TSG101 and VPS4, as well as adaptor proteins GRB2 and SOS1, and localizes to lipid rafts. In the NF-??B pathway, BST2 functions upstream of the IKK complex, I??B??, and NF-??B p65, contributing to inflammatory gene expression.
In the context of HT29 colorectal cancer cells, disruption of BST2 eliminates its intrinsic antiviral restriction and is expected to alter NF-??B-mediated inflammatory signaling. This may impact tumor cell behavior, including migration, invasion, and adhesion, thereby providing a valuable tool to dissect the role of tetherin in colorectal cancer progression. The knockout model also allows investigation of how loss of BST2 influences the interplay between innate immunity and tumorigenesis within the intestinal epithelium.
These polyclonal knockout cells are ideally suited for a wide range of research applications, including investigating mechanisms of viral infection (e.g., HIV-1), studying the contribution of BST2 to colorectal cancer pathology, and characterizing NF-??B signal transduction. Experimentally, users can perform Western blotting to assess BST2 and NF-??B pathway proteins, viral release assays to quantify viral egress, RT-qPCR to measure interferon-stimulated genes, and migration or invasion assays to evaluate tumor cell motility. Additional techniques such as co-immunoprecipitation with viral proteins, flow cytometry for surface BST2 expression, and drug sensitivity studies are compatible with this model. For further technical details or to discuss custom applications, please contact Ascent Research.
