The GPR171 Knockout CAL-27 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout population derived from the CAL-27 host cell line, featuring targeted disruption of the GPR171 gene. This loss-of-function model enables investigation of GPR171 biological roles in an oral squamous cell carcinoma background without introducing clonal selection biases. The polyclonal nature of the edited population preserves genetic heterogeneity, making it suitable for experiments where population-level responses are of primary interest.
CAL-27 is an adherent epithelial cell line isolated from a human tongue squamous cell carcinoma. It is widely employed as a tumorigenic model for oral cancer research due to its well-characterized growth properties and invasive potential. The cells exhibit typical epithelial morphology and are commonly used to study proliferation, migration, and signal transduction mechanisms in head and neck cancers.
GPR171 encodes a Gi/o-coupled G protein-coupled receptor activated by the neuropeptide-derived ligands BigLEN (PCSK1N-derived) and PEN (proSAAS-derived). Ligand binding triggers G??i/o protein coupling, which inhibits adenylyl cyclase activity and reduces intracellular cyclic AMP (cAMP) levels, thereby attenuating protein kinase A (PKA) signaling. Concurrently, GPR171 can stimulate the mitogen-activated protein kinase/extracellular signal-regulated kinase (MAPK/ERK) pathway through both G??i/o- and ??-arrestin-2-dependent mechanisms, leading to ERK1/2 phosphorylation and subsequent activation of the transcription factor cAMP response element-binding protein (CREB). Thus, GPR171 serves as a critical node linking neuropeptide signals to key second messenger systems regulating cell growth, survival, and differentiation.
In the CAL-27 oral cancer context, disruption of GPR171 is expected to perturb the balance of cAMP-PKA and MAPK/ERK signaling modules that are often dysregulated in malignancy. These pathways govern cellular proliferation, apoptosis, migration, and invasion, making the knockout model a valuable tool for dissecting the receptor??s contribution to oncogenic signaling networks. Additionally, GPR171 has been implicated in metabolic disorders and obesity, broadening the utility of this model to studies of neuropeptide signaling in cancer-relevant metabolic pathways.
This polyclonal knockout product supports a wide range of research applications, including mechanistic dissection of GPCR signaling, analysis of cAMP-PKA and ERK pathway dynamics, pharmacological validation of GPR171 as a drug target, and functional studies of oral cancer cell proliferation and migration. Representative assays include western blotting for phospho-ERK1/2 and total ERK1/2, enzyme-linked immunosorbent assays or FRET-based sensors for intracellular cAMP, colorimetric cell proliferation assays (e.g., MTS/MTT), wound healing or transwell migration assays, reverse transcription quantitative PCR for CREB target gene expression, and flow cytometric cell cycle analysis. For detailed product information and technical support, please contact Ascent Research.
