G protein-coupled receptor 141 (GPR141)

G protein-coupled receptor 141 (GPR141) is a seven-transmembrane, class A (rhodopsin-like) orphan GPCR whose endogenous ligand and many functions remain unknown. GPR141 is structurally distinctive, notably differing from canonical rhodopsin-family GPCRs in its third and seventh transmembrane domains[1]. It is widely expressed in normal and cancerous tissues, with overexpression enhancing cancer cell proliferation, migration, and invasive properties, especially in lung adenocarcinoma and breast cancer[1][2]. GPR141 modulates oncogenic signaling pathways, including suppression of p53 and activation of mTOR1, contributing to tumorigenesis and increased metastatic behavior through epithelial-mesenchymal transition (EMT). It is also implicated in immune regulation, affecting immune cell infiltration and the tumor microenvironment. While increasingly studied as a therapeutic target in cancer immunology and cell signaling research, GPR141 remains an orphan receptor with undefined physiological ligands and incomplete characterization in normal biology. No drugs currently target GPR141 directly, and its complex biology as an orphan GPCR and oncogenic driver presents both opportunities and challenges for therapeutic development[1][2].

Other names

G protein-coupled receptor 141GPCR141LOC200313

In cancers, modulation of the p-mTOR/p53 signaling pathway and regulation of epithelial-mesenchymal transition (EMT) by altering expression of mesenchymal and epithelial markers, c-Myc, VEGF, etc.[2] Functional mechanisms as an orphan GPCR, likely modulating downstream cell signaling via G protein pathways; endogenous ligand unknown[1].