This product is a CRISPR/Cas9-edited polyclonal knockout cell population derived from the NCI-H1703 human non-small cell lung carcinoma line, featuring disruption of the BTN1A1 gene. BTN1A1 encodes a butyrophilin family immunoregulatory protein that functions as a T cell co-inhibitory molecule. The polyclonal format provides a heterogeneous pool of edited cells, enabling functional studies without clonal artifacts. This loss-of-function model is designed for investigating the role of BTN1A1 in tumor?Cimmune interactions and downstream signaling networks.
The parental NCI-H1703 cell line originates from a 54-year-old Caucasian male with lung adenocarcinoma and exhibits adherent epithelial morphology. As a widely used model of non-small cell lung carcinoma, these cells retain key genetic and phenotypic features of the tumor type, making them a relevant platform for studying lung cancer biology. The host line provides a compatible cellular context for examining how BTN1A1 knockout alters tumor cell?CT cell crosstalk and intrinsic signaling properties.
BTN1A1 is a member of the butyrophilin family, structurally related to B7 co-stimulatory molecules. It functions downstream of inflammatory stimuli such as IFN-?? and TNF-??, which transcriptionally upregulate its expression via NF-??B and STAT1. BTN1A1 acts upstream of T cell receptor signaling inhibition by recruiting phosphatases SHP-1 and SHP-2, thereby suppressing ZAP70 and Lck activation at the TCR/CD3 complex. This cascade reduces IL-2 secretion and dampens T cell proliferation. BTN1A1 also interacts with xanthine oxidoreductase (XDH) and likely engages T-cell co-inhibitory receptors. Disruption of BTN1A1 thus removes a key brake on T cell activation, potentially enhancing effector functions.
In the context of NCI-H1703 lung adenocarcinoma cells, BTN1A1 knockout is predicted to abrogate negative regulation of T cells, thereby increasing anti-tumor immune responses. This model is significant for cancer immunotherapy research, particularly for studying immune checkpoint blockade and T cell co-inhibition mechanisms. Since BTN1A1 is expressed in mammary epithelium and linked to immune modulation, its deletion in a lung cancer background allows exploration of tissue-specific and tumor-specific immune evasion strategies. The model can also aid in dissecting the contributions of butyrophilin family proteins to tumor-induced immune suppression.
Researchers can employ this knockout model in a broad range of functional assays, including T cell co-cultures to assess cytokine release and cytotoxicity, western blotting to confirm protein absence, RT-qPCR for transcript levels, flow cytometry for immune checkpoint molecule profiling, and RNA-seq for transcriptomic analysis. Migration and apoptosis assays can further reveal altered tumor cell behavior. These applications support studies in cancer immunology, signal transduction, and therapeutic target validation. For additional details, please contact Ascent Research.
