The GPR171 Knockout Ca Ski Polyclonal Cells represent a CRISPR/Cas9-edited polyclonal population derived from the Ca Ski human cervical carcinoma cell line, in which the GPR171 gene has been disrupted. This loss-of-function model provides a versatile tool for investigating the biological functions of GPR171, a Gi/o-coupled GPCR, without introducing monoclonal bias. The polyclonal nature of the knockout pool retains cellular heterogeneity, closely mimicking the complexity of tumor populations and enabling robust phenotypic screening.
The parental Ca Ski cell line was established from a cervical epidermoid carcinoma metastasis in a 40-year-old Caucasian female and harbors integrated HPV-16 genomes. As a widely employed model of HPV-related cervical cancer metastasis, Ca Ski cells exhibit characteristic epithelial morphology and retain key signaling networks relevant to tumor progression. This background makes it particularly suitable for studying molecular mechanisms underlying metastatic dissemination and therapeutic resistance in cervical cancer.
GPR171 functions as a receptor for the BigLEN neuropeptide, encoded by PCSK1N, and is regulated by proSAAS. Ligand binding triggers coupling to G??i/o proteins, inhibiting adenylate cyclase and decreasing intracellular cAMP. This activates downstream effectors including PKA, MEK, ERK1/2, PI3K, and Akt, while ??-arrestin-2 and GRK2 modulate receptor desensitization. The signaling cascade influences transcription factors such as STAT3, thereby altering gene expression programs central to cell proliferation and survival.
In Ca Ski cells, GPR171-mediated signaling may synergize with HPV-16 oncoproteins to promote malignant phenotypes. The BigLEN-GPR171 axis activates MAPK/ERK and PI3K/Akt pathways, enhancing proliferation, migration, and survival. This polyclonal knockout population allows dissection of GPR171-dependent effects in an HPV-positive context, providing a relevant model for studying GPCR-driven contributions to cervical cancer progression.
Researchers can employ these cells in cAMP assays, western blotting for phospho-ERK, MTT proliferation assays, wound healing migration assays, and flow cytometry for apoptosis. RT-qPCR confirms GPR171 disruption, and xenograft studies assess in vivo tumorigenicity. Applications include preclinical drug target validation for obesity and cancer, metabolic reprogramming studies in HPV-positive cancers, and identification of novel GPCR therapeutic targets. For additional information, please contact Ascent Research.
