Songyeon Ahn

Publication Date 6-1-2025 Journal Pharmacology & Therapeutics DOI 10.1016/j.pharmthera.2025.108849 PubMedCentral® Posted Date 4-25-2026 PubMedCentral® Full Text Version Author MSS Abstract G-protein coupled receptors (GPCR) are one of the frequently investigated drug targets. GPCRs are involved in many human pathophysiologies that lead to various disease conditions, such as cancer, diabetes, and obesity. GPCR receptor activates multiple signaling pathways depending on the ligand and tissue type.

Keywords Humans, Female, Breast Neoplasms, Triple Negative Breast Neoplasms, Cell Line, Tumor, Phosphorylation, Signal Transduction, Fatty Acids, Drug Resistance, Neoplasm Abstract Approximately one-third of endocrine-treated women with estrogen receptor-alpha positive (ER+) breast cancers (BC) are at risk of recurrence due to intrinsic or acquired resistance. Thus, it is vital to understand the mechanisms underlying endocrine therapy resistance in ER+ BC to improve patient treatment.

Abstract Aggressiveness of carcinomas is linked with tumor recruitment of adipose stromal cells (ASC), which is increased in obesity. ASC promote cancer through molecular pathways not fully understood. Here, we demonstrate that epithelial–mesenchymal transition (EMT) in prostate tumors is promoted by obesity and suppressed upon pharmacological ASC depletion in HiMyc mice, a spontaneous genetic model of prostate cancer.