The GPR171 Knockout T-47D Polyclonal Cells represent a CRISPR/Cas9-edited polyclonal knockout cell population derived from the T-47D human breast ductal carcinoma cell line. This product provides a heterogeneous pool of cells carrying targeted disruptions in the GPR171 gene, generated via CRISPR/Cas9-mediated gene editing without clonal selection. The polyclonal format preserves biological variability while enabling loss-of-function studies in a physiologically relevant, hormone-responsive breast cancer background. It is supplied as a ready-to-use population, facilitating immediate integration into experimental workflows for researchers investigating GPCR signaling, tumor suppression, and endocrine therapy response mechanisms. The knockout model is designed for robust functional assays and comparative analyses with wild-type controls, supporting advanced investigations in molecular oncology and signal transduction research.
The host cell line, T-47D, is an epithelial cell line established from the pleural effusion of a 54-year-old female patient with infiltrating ductal carcinoma. These cells are characterized by estrogen receptor (ER) and progesterone receptor (PR) positivity, making them a widely employed model for hormone-dependent breast cancer studies. T-47D cells exhibit adherent morphology and retain key features of luminal breast cancer, including sensitivity to estrogen and anti-estrogen therapies. Their well-documented molecular profile and stable growth characteristics provide a consistent and disease-relevant platform for evaluating gene function in the context of endocrine signaling. The use of this cell line as the knockout background ensures that observations from GPR171 disruption are interpreted within a clinically meaningful breast cancer paradigm.
GPR171 encodes a G protein-coupled receptor that functions as a receptor for the neuropeptide Big LEN. It is primarily coupled to G??i/o proteins, and upon ligand activation, it inhibits adenylyl cyclase activity, leading to reduced intracellular cAMP levels and diminished protein kinase A (PKA) signaling. This cascade modulates multiple downstream effectors, including the transcription factor CREB and, putatively, ERK1/2. The receptor is regulated by upstream factors such as the Big LEN peptide, proSAAS, and potentially by estrogen signaling. Interacting partners include G??i/o, beta-arrestin, and G protein-coupled receptor kinases (GRKs). Mechanistically, GPR171 operates within the canonical GPCR?CGi/o?Cadenylyl cyclase?CcAMP?CPKA?CCREB axis, thereby influencing transcriptional programs linked to cellular proliferation and metabolism.
In the T-47D knockout model, disruption of GPR171 allows dissection of its role in hormone-responsive breast cancer cell biology. Given the putative tumor-suppressive functions of GPR171, the knockout population may exhibit altered proliferative, migratory, and invasive behaviors, providing insight into how loss of this receptor impacts cancer cell phenotypes under estrogenic stimulation. The model is particularly valuable for studying crosstalk between neuropeptide signaling and the endocrine network, as well as for validating GPR171 as a therapeutic target or biomarker. By comparing knockout and wild-type T-47D cells, researchers can delineate GPR171-dependent changes in cAMP dynamics, CREB transcriptional activity, and sensitivity to anti-estrogens, thereby elucidating the receptor’s contribution to breast cancer progression and treatment response.
This polyclonal GPR171 knockout product is ideally suited for a broad range of research applications, including breast cancer pathobiology, GPCR signal transduction, drug target validation, and metabolic disorder studies. Investigators can employ assays such as Western blotting to confirm GPR171 protein loss, RT-qPCR for knockout validation, and cAMP accumulation assays to assess Gi/o pathway functionality. Functional readouts may include MTT proliferation assays, migration and invasion tests, and RNA-seq transcriptomic profiling to capture global gene expression changes. Additionally, the model enables drug sensitivity testing to explore endocrine therapy responses in a GPR171-deficient context. For additional technical specifications and ordering information, please contact Ascent Research.
