The KLRB1 Knockout MCF-7 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population derived from the MCF-7 human breast adenocarcinoma cell line, featuring targeted disruption of the KLRB1 gene. This polyclonal pool contains a mixture of cells with various editing events, providing a population-level gene disruption model without clonal selection. The knockout is generated using CRISPR/Cas9 technology, resulting in loss-of-function of the encoded CD161 protein.
MCF-7 is a well-characterized breast cancer cell line established from the pleural effusion of a 69-year-old Caucasian female with metastatic adenocarcinoma. It is estrogen receptor (ER)-positive, progesterone receptor (PR)-positive, and human epidermal growth factor receptor 2 (HER2)-negative, representing the luminal A molecular subtype. This hormone-responsive line is extensively utilized in cancer biology research, particularly for studying endocrine therapy resistance, tumor cell signaling, and cellular responses to hormonal stimuli.
KLRB1 encodes CD161, a C-type lectin-like inhibitory receptor that interacts with its ligand LLT1 (CLEC2D). In immune cells, CD161 engagement recruits the tyrosine phosphatases SHP-1 (PTPN6) and SHP-2 (PTPN11), which dephosphorylate key signaling molecules such as ZAP70 and LCK, leading to inhibition of NK cell cytotoxicity and reduced secretion of IFN-?? and TNF-??. The CD161-LLT1 axis functions as an immune checkpoint, and its signaling involves downstream effectors including PI3K/AKT and ERK/MAPK pathways. Upstream, CD161 expression is regulated by cytokines like IL-15 and transcription factors STAT4 and T-bet. In the context of MCF-7 cells, CD161 may modulate intracellular signaling networks that influence tumor cell behavior.
Knocking out KLRB1 in MCF-7 cells provides a powerful tool to dissect the cell-intrinsic roles of CD161 in breast cancer. Since MCF-7 cells express LLT1, autocrine or paracrine CD161-LLT1 interactions might contribute to tumor cell proliferation, survival, or immune modulation. This knockout model enables investigation of CD161-dependent signaling cascades and their impact on hormone responsiveness, migration, and interaction with immune effectors. The use of a polyclonal population avoids clonal artifacts and better represents the heterogeneous responses seen in tumor biology.
Researchers can employ this knockout model in co-culture assays with primary NK cells or CD161-expressing T cells to study immune evasion mechanisms, measuring cytotoxicity by LDH release or cytokine production via ELISA. The cells are suitable for phospho-kinase profiling to map CD161-mediated signaling alterations, migration and invasion assays using Transwell systems, and proliferation studies with MTT or BrdU. Transcriptomic analyses by RNA-seq can reveal global gene expression changes upon KLRB1 disruption. This product is ideal for screening CD161-targeted immunotherapies and understanding tumor-immune crosstalk in breast cancer. For additional information or to place an order, please contact Ascent Research.
