The BTN1A1 Knockout KYSE-150 Polyclonal Cells represent a CRISPR/Cas9-edited human polyclonal knockout cell population designed for loss-of-function studies of the BTN1A1 gene. This product provides a heterogeneous pool of edited cells, avoiding clonal selection artifacts and enabling robust investigation of BTN1A1-dependent functions within a tumor-relevant background. The polyclonal format captures the genetic diversity inherent in CRISPR-mediated disruption, making it suitable for assays that require population-level responses consistent with native tumor heterogeneity. Researchers can employ this model to dissect the contributions of BTN1A1 to immune modulation and lipid metabolism directly in esophageal squamous cell carcinoma cells.
The parental KYSE-150 cell line is an epithelial model established from the poorly differentiated esophageal squamous cell carcinoma of a Japanese female patient. These cells retain hallmark features of esophageal cancer, including deregulated growth signaling and invasive potential, and are widely utilized to study the molecular pathology of esophageal malignancies. Their genetic background and tumorigenic properties offer a clinically relevant platform for probing gene function in the context of esophageal squamous cell carcinoma. By introducing BTN1A1 knockout into this system, the impact of the target gene can be examined against a well-characterized oncogenic landscape.
BTN1A1 encodes a transmembrane butyrophilin family protein that performs dual roles in lipid secretion and immune checkpoint regulation. Mechanistically, BTN1A1 interacts with xanthine oxidoreductase (XDH) to facilitate milk fat globule secretion in mammary cells, while in immune tissues it is thought to engage T cell receptors and co-receptors such as CD3 and CD28, potentially delivering inhibitory signals that attenuate T cell activation. The gene is downstream of prolactin receptor signaling via JAK2 and STAT5, and it modulates the activity or expression of XDH and perilipin-2. These molecular connections place BTN1A1 at the intersection of lipid handling and adaptive immunity, making its disruption a valuable tool for functional dissection of these networks.
In the KYSE-150 background, BTN1A1 knockout allows targeted investigation of its putative immune checkpoint properties within the esophageal tumor microenvironment. Given the observed upregulation of butyrophilins in certain cancers and their potential to facilitate immune evasion, this model is particularly relevant for examining how BTN1A1 contributes to T cell suppression in esophageal squamous cell carcinoma. Additionally, because BTN1A1 is linked to milk fat globule secretion and perilipin-2, the knockout cells provide a system to explore lipid droplet dynamics and metabolism in cancer cells, which are increasingly recognized as hallmarks of aggressive tumors. The polyclonal nature ensures that the cellular responses observed are not biased by single-cell expansion artifacts.
This knockout product supports a range of experimental applications critical for cancer biology and immunology research. Genotyping PCR and anti-BTN1A1 western blotting can be used to confirm gene disruption and protein loss. Functional studies may include T cell co-culture and activation assays to measure changes in immune checkpoint activity, as well as BODIPY staining to visualize lipid droplets. Transcriptomic profiling via RNA-seq enables pathway-level assessment of BTN1A1 loss, while migration and invasion assays reveal its impact on metastatic potential. These applications position the BTN1A1 Knockout KYSE-150 Polyclonal Cells as a flexible resource for dissecting both tumor-intrinsic and immune-modulatory roles of BTN1A1. For further technical information or to arrange access, please contact Ascent Research.
