The KLRB1 Knockout HGC-27 Polyclonal Cells constitute a CRISPR/Cas9-mediated gene-disrupted cell population designed for functional studies of the CD161-encoding gene KLRB1 in a human gastric cancer background. This polyclonal knockout product eliminates wild-type KLRB1 expression through targeted genome editing, providing a heterogeneous loss-of-function model without clonal selection. The knockout cells are generated from the HGC-27 parental line and serve as a versatile tool for dissecting the role of CD161 in immune receptor signaling, tumor cell-intrinsic pathways, and interactions with the tumor microenvironment.
The parental HGC-27 cell line is a widely used adherent model of human gastric adenocarcinoma, originally established from the lymph node metastasis of an undifferentiated gastric carcinoma. HGC-27 cells retain key features of gastric cancer biology, including aberrant proliferative signaling and invasive potential, making them suitable for investigating molecular mechanisms underpinning gastric tumorigenesis. The knockout population is maintained under standard culture conditions and exhibits morphological and growth characteristics consistent with the parental line, with the specific ablation of KLRB1 enabling functional comparisons.
KLRB1 encodes CD161, an inhibitory C-type lectin receptor expressed on NK cells and T cells. Binding to LLT1 recruits SHP-1 and SHP-2 phosphatases via its ITIM, which dephosphorylate Lck and ZAP70, thus attenuating activation. In gastric tumor cells, CD161 may modulate PI3K-AKT and NF-??B signaling, altering IFN-?? and TNF-?? production. KLRB1 expression is upregulated by IL-2, IL-15, NF-??B, and AP-1. The receptor also interacts with Grb2, LAT, and SHIP-1, intersecting JAK-STAT and immune checkpoint pathways.
In gastric cancer, KLRB1 expression on tumor cells or infiltrating immune cells may contribute to immune evasion by dampening anti-tumor responses. The HGC-27 KLRB1 knockout model enables researchers to separate the cell-autonomous effects of CD161 loss on tumor proliferation, survival, and migration from its immunomodulatory functions. This system is particularly relevant for studying the crosstalk between gastric carcinoma cells and components of the tumor microenvironment, including the LLT1?CCD161 immune checkpoint axis. It also provides a platform to investigate how loss of CD161 alters sensitivity to chemotherapy or targeted agents, given the involvement of the PI3K-AKT and NF-??B pathways.
Typical applications include RT-qPCR and western blotting to confirm knockout and assess downstream targets, flow cytometry for surface profiling, and phospho-signaling analysis to map pathway alterations. The polyclonal population is suitable for cytotoxicity, migration, and invasion assays, as well as co-cultures with immune cells. Cytokine ELISA and co-immunoprecipitation enable quantification of secreted factors and protein interactions. The cells also support screening of compounds targeting CD161 or downstream nodes. For further information, please contact Ascent Research.
