The BTN1A1 Knockout SK-OV-3 Polyclonal Cells product is a heterogeneous population of SK-OV-3 human ovarian adenocarcinoma cells engineered via CRISPR/Cas9-mediated disruption of the BTN1A1 gene. This polyclonal knockout pool retains diverse editing events across the cell population, providing a robust loss-of-function model for studying BTN1A1 in the context of epithelial ovarian cancer. The cells are cryopreserved immediately after editing and validation, ensuring a ready-to-use reagent for functional genomics, immune checkpoint investigation, and cancer cell biology. As a polyclonal knockout, the population reflects the biological variability inherent in CRISPR/Cas9 gene targeting, making it suitable for pooled screening or bulk assays where population-level effects are of primary interest.
The host cell line SK-OV-3 is a widely studied human ovarian adenocarcinoma epithelial line originally derived from the ascites of a patient with progressive ovarian carcinoma. These cells are p53-deficient and exhibit resistance to tumor necrosis factor as well as several chemotherapeutic agents, including cisplatin and adriamycin. SK-OV-3 serves as a canonical model for high-grade serous ovarian cancer, displaying characteristic epithelial morphology and invasive properties. Its well-documented genetic background and established use in drug resistance and metastasis research make it a relevant platform for exploring the functions of immune-modulatory and metabolic genes such as BTN1A1.
BTN1A1 encodes a type I transmembrane glycoprotein belonging to the butyrophilin family of the immunoglobulin superfamily, which shares structural homology with the B7 family of co-stimulatory/co-inhibitory molecules. In mammary epithelial tissues, BTN1A1 is transcriptionally regulated by prolactin and glucocorticoids via STAT5 and NF-??B signaling, and it orchestrates milk fat globule secretion by bridging cytoplasmic lipid droplets to the apical plasma membrane through a direct interaction with xanthine dehydrogenase (XDH) and perilipin-2. In immune contexts, butyrophilins are recognized as co-inhibitory receptors, and BTN1A1 has been implicated in modulating T cell activity by engaging T cell receptors and recruiting the phosphatase SHP-1 to dampen activation signals. Knockout of BTN1A1 therefore disrupts both lipid secretion pathways and potential immune checkpoint interactions, providing multifaceted insights.
In SK-OV-3 ovarian cancer cells, BTN1A1 knockout offers a unique model to dissect its dual roles in lipid metabolism and immune evasion. The p53-null, chemoresistant background of SK-OV-3 enables investigation of how BTN1A1 contributes to tumor cell-intrinsic survival signals and to the suppression of anti-tumor T cell responses. Because BTN1A1 may function as a checkpoint molecule, its disruption in this ovarian carcinoma line can facilitate studies on reversing T cell inhibition, potentially enhancing IFN-?? production in co-culture assays. Furthermore, the knockout allows examination of altered lipid droplet dynamics and XDH-dependent metabolic pathways in a cancer context where lipid reprogramming is linked to malignancy.
This polyclonal knockout cell product is designed for a range of advanced applications, including functional assessment of BTN1A1 in ovarian cancer immune escape using T cell co-culture and IFN-?? release assays, quantitative analysis of BTN1A1 mRNA and protein expression via RT-qPCR and western blotting, and evaluation of cancer cell migration and invasion properties. Flow cytometric profiling of immune checkpoint markers further enables characterization of the immunomodulatory landscape following BTN1A1 disruption. Researchers can also employ these cells to screen for compounds that target the BTN1A1?CXDH interaction or STAT5/NF-??B-regulated pathways. For further information or to discuss custom applications, please contact Ascent Research.
