The BTN1A1 Knockout HGC-27 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population designed to disrupt the BTN1A1 gene in the HGC-27 human gastric adenocarcinoma cell line. This polyclonal loss-of-function model avoids clonal isolation and enables study of BTN1A1-dependent functions across a diverse genetic background, suitable for population-level analyses.
HGC-27 is an epithelial cell line derived from lymph node metastasis of a histiocytic-like gastric carcinoma. It is tumorigenic in immunodeficient mice and widely employed to model gastric adenocarcinoma, including studies of tumor progression, metastasis, and therapeutic interventions.
BTN1A1 encodes a transmembrane glycoprotein that mediates milk fat globule secretion in mammary cells via interaction with xanthine oxidoreductase (XOR), downstream of perilipin-2 (PLIN2). In immune contexts, BTN1A1 acts as a co-inhibitory checkpoint molecule on cancer cells, engaging an unknown T cell inhibitory receptor to suppress TCR-mediated activation. This reduces IL-2 and IFN-?? production through ERK signaling, regulated upstream by STAT5 and NF-??B in response to cytokines like TNF-?? and IFN-??.
In HGC-27 gastric cancer cells, BTN1A1 likely promotes immune evasion by inhibiting anti-tumor T cell responses. Knocking out BTN1A1 allows dissection of its immune-modulatory role independently of its lipid secretion function. Researchers can examine how loss of BTN1A1 alters T cell proliferation, cytokine profiles, and tumor growth in xenograft models, providing insight into butyrophilin-mediated immune checkpoints in the gastric tumor microenvironment.
This product supports applications in immunology and cancer biology, including Western blotting and RT-qPCR for knockout validation, flow cytometry for surface marker analysis, and co-immunoprecipitation of BTN1A1?CXOR complexes. Functional assays such as T cell proliferation and ELISA for IL-2 and IFN-?? quantify immune checkpoint activity, while migration, invasion, and xenograft studies assess tumor behavior. For further details, please contact Ascent Research.
