The BTN1A1 Knockout MCF-7 Polyclonal Cells product provides a CRISPR/Cas9-edited polyclonal cell population with targeted disruption of the BTN1A1 gene in the MCF-7 human breast adenocarcinoma epithelial cell line. This heterogeneous knockout pool enables loss-of-function studies of butyrophilin subfamily 1 member A1, a transmembrane immunoglobulin superfamily protein implicated in lipid secretion and immune modulation. The polyclonal format yields a diverse range of gene-edited cells, making it well-suited for population-based assays that interrogate BTN1A1-dependent biological processes without requiring clonal isolation.
The MCF-7 host cell line is a widely characterized model of estrogen receptor-positive (ER+), progesterone receptor-positive (PR+) luminal A breast cancer, originally derived from the pleural effusion of a 69-year-old Caucasian female with metastatic adenocarcinoma. These cells retain wild-type p53 status, epithelial morphology, and hormone responsiveness, enabling physiologically relevant investigations of signaling pathways and metabolic functions within a breast epithelial context. Their extensive use in cancer biology, drug development, and endocrine research provides a robust experimental background for gene disruption studies.
BTN1A1 is transcriptionally regulated by prolactin and glucocorticoids, acting through STAT5 and NF-??B signaling, and encodes a protein that orchestrates milk fat globule secretion by recruiting xanthine oxidoreductase (XDH) and perilipin-2 (PLIN2) to the apical plasma membrane, facilitating lipid droplet envelopment and release. Additionally, BTN1A1 interacts with BTN2A2 and cytoskeletal components, and may engage T cells via butyrophilin-mediated immune modulation, thereby influencing immune tolerance or activation. Downstream, BTN1A1 promotes XDH activation and PLIN2 association, processes critical for lipid secretion and potentially for broader cellular lipid handling.
In the MCF-7 breast cancer model, BTN1A1 knockout provides a valuable system for dissecting the gene??s contributions to lipid droplet biology and butyrophilin-mediated immune interactions beyond its canonical lactation role. Although MCF-7 cells are not lactogenic, they retain epithelial characteristics and express hormone receptors that may modulate BTN1A1 expression, making them suitable for studying how hormone-driven BTN1A1 activity could influence lipid metabolism, cellular energetics, or tumor microenvironment crosstalk in breast cancer. This system enables examination of whether BTN1A1 participates in processes such as lipid droplet formation, membrane trafficking, or immune evasion strategies relevant to cancer progression.
Researchers can employ this knockout pool in diverse applications, including Western blot and RT-qPCR confirmation of BTN1A1 disruption, immunofluorescence visualization of lipid droplets, flow cytometric analysis of surface markers, and phospho-signaling assessments of STAT5 and NF-??B pathways. Lipid secretion assays and co-immunoprecipitation with XDH or PLIN2 can elucidate functional interactions, while migration, invasion, and drug sensitivity studies (e.g., tamoxifen response) may reveal BTN1A1??s role in breast cancer cell behavior. This reagent supports drug screening for BTN1A1-targeted therapies and investigations into butyrophilin-mediated immune modulation. For further details, please contact Ascent Research.
