CaSR, the calcium-sensing receptor, is a class-C G protein-coupled receptor. It plays a pivotal role in regulating calcium homeostasis by sensing extracellular Ca2+ concentration changes. It is also involved in various other cellular processes such as gene transcription, cell proliferation, differentiation, apoptosis, muscle contraction, and neuronal transmission. The CaSR-mediated intracellular Ca2+ signaling is part of key biological pathways [2].

In conditional and global CaSR knockout mice, colonic epithelia showed increased proliferation with enhanced Wnt/β-catenin signaling, indicating that CaSR negatively modulates colonic epithelial growth [3]. In breast cancer, CaSR acts as an oncoprotein and drives the pathogenesis of skeletal metastases. Understanding the CaSR signaling in this context could lead to novel therapeutic interventions for metastatic breast cancer [1,5]. Mutations in the CASR gene cause autosomal dominant hypocalcemia type 1 (ADH1), characterized by hypocalcemia, low parathyroid hormone levels, and high urinary calcium [4].

In conclusion, CaSR is crucial for calcium homeostasis and various cellular functions. Gene knockout mouse models have revealed its role in colonic epithelial growth regulation and in the pathogenesis of breast cancer bone metastases and ADH1. Research on CaSR provides insights into the molecular basis of these disease conditions and may facilitate the development of targeted therapeutic agents.