GPR52 (G Protein-Coupled Receptor 52)

Overall, our results reveal GPR52 loss as a potential mechanism by which breast cancer progression may occur and support the investigation of GPR52 agonism as a therapeutic option in breast cancer. We show that loss of the orphan G protein-coupled receptor GPR52 in human breast cell lines leads to increased cell clustering, hybrid/partial EMT, and increased tumor burden in zebrafish.

High-fat diet (HFD)-induced increase in hepatic expression of Pparg2 and its targets (Scd1 and Elovl6) was absent in Gpr52 mice with alleviated hepatosteatosis. Our present study showed that hepatic GPR52 promotes the biosynthesis of fatty acid and cholesterol in a ligand-dependent and a constitutive manner, respectively, and Gpr52 participates in HFD-induced fatty acid synthesis in liver.

We used a multi-omics approach to profile metastatic tumor tissues and serial blood samples from 47 mCRC patients who received single-agent regorafenib as second-line therapy after failing first-line therapy with an oxaliplatin or irinotecan-containing regimen with or without bevacizumab. The profiling of plasma samples showed a higher proportion of samples with non-detectable ctDNA in patients exhibiting longer PFS (PFS ≥ 9 months, 70%) compared to patients with shorter PFS (< 9 months, 18%). This study allowed the identification of several candidate genes and regions at different molecular levels that warrant further validation in order to stratify patients who will likely respond, display intrinsic resistance or develop acquired resistance to regorafenib treatment.