The KLRB1 Knockout KYSE-150 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population derived from the human esophageal squamous cell carcinoma cell line KYSE-150. This product features a targeted disruption of the KLRB1 gene, which encodes the C-type lectin-like receptor CD161, creating a loss-of-function model to investigate CD161-mediated cellular processes. As a polyclonal population, these cells provide a heterogeneous mix of knockout genotypes, enabling robust functional studies without the biases of single-cell clonal selection. This tool is designed to dissect the roles of KLRB1 in immune regulation and cancer biology.
The parental KYSE-150 cell line was established from a poorly differentiated human esophageal squamous cell carcinoma and is extensively used in cancer research. These epithelial cells retain hallmark characteristics of the original tumor, including dysregulated growth signaling and aggressive behavior, making them an appropriate model for esophageal cancer biology. The KLRB1 knockout in this background offers a clinically relevant system to study CD161 function within the context of esophageal squamous cell carcinoma, particularly its influence on tumor cell signaling and interactions with the immune microenvironment.
KLRB1 encodes the receptor CD161, a C-type lectin-like molecule that interacts with its ligand LLT1 (CLEC2D). Upon engagement, CD161 recruits ITIM-containing adaptors and SHP-1/SHP-2 phosphatases, which in turn modulate key signaling cascades, including PI3K/AKT/mTOR, MAPK/ERK, and NFAT pathways. This signaling regulates the secretion of effector cytokines such as IFN-?? and TNF-??, as well as the release of cytotoxic granules. Upstream regulators of KLRB1 include cytokines IL-12, IL-15, and IL-2, along with transcription factors T-bet and Eomes. In epithelial cancer cells, CD161 may transmit signals that alter cell proliferation, survival, and immune recognition through LLT1-mediated crosstalk.
In the KYSE-150 esophageal squamous cell carcinoma model, disrupting KLRB1 allows precise interrogation of CD161??s contributions to tumor-intrinsic pathways and tumor-immune interactions. Esophageal squamous cell carcinoma progression often involves immune evasion, and the CD161-LLT1 axis may play a role in modulating the tumor microenvironment. By abrogating CD161 expression, researchers can examine changes in cellular signaling, cytokine output, and susceptibility to immune effector cells such as NK cells and T lymphocytes. This provides a platform to explore how CD161 facilitates immune escape and to identify potential therapeutic targets.
This polyclonal KLRB1 knockout cell population is suitable for a broad range of experimental applications, including functional characterization of CD161 in esophageal cancer, tumor-immune co-culture assays to measure lymphocyte-mediated cytotoxicity, cytokine secretion profiling (e.g., IFN-??, TNF-??), and phospho-signaling analysis of AKT and ERK activation. It also enables drug target validation and high-content screening for modulators of CD161-dependent phenotypes. Routine validation can be performed by western blotting, RT-qPCR, or flow cytometry for CD161 surface expression. For additional information and technical support, please contact Ascent Research.
