The GPR171 Knockout SK-OV-3 Polyclonal Cells consist of a polyclonal population of SK-OV-3 human ovarian adenocarcinoma cells engineered via CRISPR/Cas9-mediated gene disruption to eliminate GPR171 expression. This pool of edited cells contains a spectrum of loss-of-function alleles, providing a robust knockout model free from clonal selection artifacts. Researchers can utilize this reagent to investigate GPR171 function in signaling, cancer biology, and pharmacological studies.
The SK-OV-3 parental cell line, isolated from the ascitic fluid of a 64-year-old ovarian adenocarcinoma patient, is a well-established epithelial ovarian cancer model. It exhibits tumorigenicity in nude mice and resistance to cisplatin, characteristics that make it valuable for studying drug resistance and tumor progression. The ovarian cancer lineage offers a disease-relevant platform for probing GPR171-mediated effects.
GPR171 is an orphan class A GPCR activated by the BigLEN neuropeptide. Upon ligand binding, it engages G??i/o proteins to inhibit adenylyl cyclase, decreasing cAMP production and attenuating downstream PKA and CREB signaling. It also interacts with ??-arrestin 1 and ??-arrestin 2, which regulate receptor trafficking and alternative signaling routes. Key pathway components include the receptor, BigLEN, G??i/o, adenylyl cyclase, cAMP, PKA, and CREB, forming a canonical GPCR cascade.
In ovarian cancer cells, GPR171 is thought to function as a tumor suppressor, and its knockout may derepress proliferative and survival pathways. Disruption of this signaling node in SK-OV-3 cells allows dissection of how cAMP/PKA/CREB modulation influences malignant properties such as growth, apoptosis, and migration, thereby contributing to a deeper understanding of ovarian adenocarcinoma biology.
Typical applications include orphan receptor deorphanization, neuropeptide signaling studies, and GPCR target validation. Compatible assays range from molecular confirmation (RT-qPCR, western blot) and cAMP quantification to functional analyses of proliferation (CCK-8), apoptosis (Annexin V), colony formation, migration (Transwell), and phospho-CREB measurement. In vivo tumor xenograft models further enable preclinical assessment. For additional information, contact Ascent Research.
