The BTN1A1 Knockout HCT 116 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal population derived from the HCT 116 colorectal carcinoma line, designed to disrupt the butyrophilin subfamily 1 member A1 (BTN1A1) gene. This loss-of-function model provides a heterogeneous pool of edited cells, enabling functional studies without clonal selection bias.
HCT 116 is a human colorectal carcinoma epithelial line carrying a KRAS G13D mutation and activating CTNNB1 mutations, combined with MLH1 deficiency and high microsatellite instability (MSI-H). This MSI-H status reflects defective DNA mismatch repair, making the line particularly suited for immuno-oncology research and studies of tumor-intrinsic signaling pathways.
BTN1A1 is a butyrophilin family member of the immunoglobulin superfamily that modulates T cell responses and has been proposed as a T cell co-inhibitory molecule. Its expression is regulated by STAT5, NF-??B, and prolactin. BTN1A1 interacts with xanthine dehydrogenase/oxidase (XDH) and influences lipid droplet-associated proteins, linking it to lipid metabolism. In T cell receptor signaling, BTN1A1 may intersect with CD3 and ZAP70, positioning it as a potential modulator of immune activation thresholds.
Knockout of BTN1A1 in the MSI-H HCT 116 context creates a relevant model for examining immune checkpoint regulation in colorectal carcinoma. The high mutational burden of MSI-H tumors underscores the value of this polyclonal knockout for dissecting BTN1A1??s contributions to tumor immune evasion, cytokine milieu, and metabolic crosstalk within the tumor microenvironment.
Applications include co-culture assays with T cells to quantify immune checkpoint activity, western blotting for XDH interaction, RT-qPCR for BTN1A1 expression, flow cytometry for T cell activation markers, and lipid droplet staining. Researchers can employ this model for mechanistic studies of butyrophilin-mediated immune modulation, therapeutic target screening, and phospho-signaling analysis in colorectal cancer biology. For further information, please contact Ascent Research.
