Gpr160, an orphan G-protein-coupled receptor (GPCR), has been associated with multiple biological functions. It has been implicated in regulating the self-renewal and pluripotency of mouse embryonic stem cells via the JAK1/STAT3 signaling pathway [1]. Additionally, it may play roles in pain-related processes and potentially in cancer-related mechanisms [2,3].

In rodent models, Gpr160 gene knockout (KO) mice fail to develop behavioral hypersensitivities in a neuropathic pain model caused by sciatic nerve constriction. Also, the development of behavioral hypersensitivities after intrathecal or intraplantar injections of cocaine-and amphetamine-regulated transcript peptide (CARTp) is dependent on Gpr160, suggesting its pronociceptive role [4]. In glioma, knockdown of Gpr160 inhibits proliferation, colony formation, and cell viability, and promotes apoptosis, indicating its potential as a therapeutic target in glioma [3]. In bone cancer pain models, targeted interventions of Gpr160 mitigate mechanical allodynia, cold, and heat hyperalgesia [2].

In conclusion, Gpr160 is involved in the regulation of stem cell self-renewal and pluripotency, and plays important roles in pain-related behaviors and potentially in cancer-related processes. The use of Gpr160 KO mouse models has been crucial in revealing its functions in neuropathic pain and glioma-related processes, providing insights for potential therapeutic interventions in these disease areas.

References:

1. Fan, Shasha, Guo, Chuanliang, Yang, Guanheng, Xue, Yan, Zeng, Fanyi. 2024. GPR160 regulates the self-renewal and pluripotency of mouse embryonic stem cells via JAK1/STAT3 signaling pathway. In Journal of genetics and genomics = Yi chuan xue bao, 51, 1055-1065. doi:10.1016/j.jgg.2024.05.003. https://pubmed.ncbi.nlm.nih.gov/38750952/

2. Xu, Chengfei, Wang, Yahui, Ni, Chaobo, Yao, Ming, Ni, Huadong. 2024. Histone modifications and Sp1 promote GPR160 expression in bone cancer pain within rodent models. In EMBO reports, 25, 5429-5455. doi:10.1038/s44319-024-00292-6. https://pubmed.ncbi.nlm.nih.gov/39448865/

3. Abbas, Azar, Jun, Peng, Yuan, Jiang Yuan, Jiang, Jinwei, Yuan, Shengtao. 2022. Downregulation of GPR160 inhibits the progression of glioma through suppressing epithelial to mesenchymal transition (EMT) biomarkers. In Basic & clinical pharmacology & toxicology, 131, 241-250. doi:10.1111/bcpt.13769. https://pubmed.ncbi.nlm.nih.gov/35771163/

4. Schafer, Rachel M, Giancotti, Luigino A, Davis, Daniel J, Farr, Susan A, Salvemini, Daniela. 2024. Behavioral characterization of G-protein-coupled receptor 160 knockout mice. In Pain, 165, 1361-1371. doi:10.1097/j.pain.0000000000003136. https://pubmed.ncbi.nlm.nih.gov/38198232/