The GPR171 Knockout HGC-27 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population generated from the human gastric adenocarcinoma cell line HGC-27, featuring targeted disruption of the GPR171 gene. This polyclonal pool consists of a heterogeneous mix of edited cells carrying CRISPR/Cas9-mediated gene disruption at the GPR171 locus, providing a collective loss-of-function model without single-cell cloning. The product is supplied as a polyclonal population to preserve genetic diversity and functional knockout representation across the culture.
The HGC-27 cell line is a well-characterized human gastric carcinoma cell line originally established from a metastatic lymph node of a gastric adenocarcinoma patient. It is widely employed as an in vitro model for studying gastric cancer biology, including tumorigenesis, metastasis, and drug response. The epithelial origin and metastatic derivation of HGC-27 make it particularly relevant for research on advanced gastric cancer and the molecular mechanisms underlying tumor progression.
GPR171 encodes a Gi/o-coupled receptor that is specifically activated by the BigLEN neuropeptide, a processed product of the proSAAS precursor. Upon ligand binding, GPR171 couples to the Gi/o protein alpha subunit, leading to inhibition of adenylyl cyclase and a consequent reduction in intracellular cAMP levels. The resulting attenuation of cAMP-dependent protein kinase A (PKA) activity diminishes phosphorylation of the transcription factor CREB. Additionally, GPR171 signaling engages ERK1/2 pathways and recruits beta-arrestin, which can modulate receptor desensitization and downstream scaffolding functions. Through these interactions, GPR171 serves as a pivotal link connecting neuropeptide stimulation to intracellular second-messenger cascades and transcriptional responses.
In the HGC-27 gastric cancer cell line, GPR171 may contribute to processes such as proliferation and migration, key hallmarks of malignant progression. As a Gi/o-coupled receptor potentially modulating these phenotypes, GPR171 represents an experimental target for studying GPCR signaling in gastric adenocarcinoma. The polyclonal knockout model enables assessment of global loss-of-function effects without clonal selection bias, offering a more representative view of GPR171??s role in a metastatic gastric cancer background. This model is well-suited for dissecting the receptor??s involvement in growth factor-independent signaling or crosstalk with oncogenic pathways.
This polyclonal knockout cell population supports diverse functional assays, including MTT viability tests, BrdU proliferation assays, Transwell migration assays, and Annexin V apoptosis detection. For signaling studies, researchers can perform cAMP ELISA, CREB luciferase reporter assays, and western blotting for phospho-CREB to quantify GPR171-mediated pathway modulation. RT-qPCR analysis of downstream gene expression can further elucidate transcriptional effects. These cells are also suitable for drug screening of GPR171 modulators and as a negative control for BigLEN stimulation experiments. For additional information, please contact Ascent Research.
