mProX™ Human GPR50 Stable Cell Line

Nolan PM, et al. "A missense mutation in zinc finger homeobox-3 (ZFHX3) impedes growth and alters ." FASEB journal : official publication of the Federation of American Societies for , 2023.
A recent human genome-wide association study found that a protein altering variant in the gene encoding zinc finger homeobox-3 (ZFHX3) is associated with lower BMI. In this study, the researchers investigated the metabolic parameters in mice with a missense mutation in Zfhx3 (Zfhx3(Sci/+)) to understand how ZFHX3 may affect growth and metabolism. The results showed that one-year-old male and female Zfhx3(Sci/+) mice had lower weight, body length, fat mass, and circulating insulin, leptin, and insulin-like growth factor-1 levels compared to wildtype littermates. In a separate cohort, Zfhx3(Sci/+) mice consumed less food in proportion to their body weight. Furthermore, female Zfhx3(Sci/+) mice had lower lean mass and energy expenditure, but not fat mass, compared to Zfhx3(+/+) mice. The researchers also observed altered expression of key neuropeptides involved in energy balance, such as somatostatin, growth hormone-releasing hormone, growth hormone-receptor, neuropeptide Y, and orphan G protein-coupled receptor Gpr50, in the arcuate nucleus (ARC) and ventricular ependymal regions of the Zfhx3(Sci/+) mice. These findings suggest that the Zfhx3(Sci) mutation may have an impact on energy balance by altering the expression of key neuropeptides in the ARC. This study is the first to demonstrate an effect of the Zfhx3(Sci) mutation on energy balance and sheds light on the potential mechanisms by which ZFHX3 may influence growth, food intake, and energy expenditure.
Pubmed: 37713040   DOI: 10.1096/fj.202201829R

Zhao W, et al. "High expression of GPR50 promotes the proliferation, migration and autophagy of ." Journal of cell communication and signaling, 2023.
G-protein coupled receptors (GPCRs) have been shown to play a key role in tumorigenesis and the development of hepatocellular carcinoma (HCC). Among these receptors, GPR50, an orphan GPCR, has been identified as a potential protector against breast cancer development and an inhibitor of tumor growth in a xenograft mouse model. However, its role in HCC remains unclear. To investigate this, the authors analyzed GPR50 expression in HCC patients utilizing the Gene Expression Omnibus database (GSE45436) and in the HCC cell line CBRH-7919. Results showed that GPR50 expression was significantly higher in HCC patients and in CBRH-7919 cells compared to respective normal controls. By transfecting Gpr50 cDNA into CBRH-7919, the authors observed increased proliferation, migration, and autophagy of the cells. Further analysis using isobaric tags for relative and absolute quantification (iTRAQ) revealed that GPR50 may promote HCC progression through the upregulation of CCT6A-induced proliferation and PGK1-induced migration and autophagy. This suggests that targeting GPR50 could have potential therapeutic implications for HCC.
Pubmed: 37378811   DOI: 10.1007/s12079-023-00772-9