Gpr162, an orphan receptor in the G-protein-coupled receptor family, has diverse functions. It may be involved in regulating intercellular interactions related to physiological processes such as food intake, glucose homeostasis, and hormonal sensing signaling [3,4]. It also plays a role in the central nervous system (CNS) and is associated with some diseases.

In cancer research, overexpression of Gpr162 can interact with the stimulator of interferon genes (STING), target DNA damage responses, activate IRF3, accelerate the activation of the type I interferon system, promote chemokine expression (like CXCL10 and CXCL4), and inhibit tumor occurrence and development. STING inhibitors can counteract the antitumor effect of Gpr162 overexpression in IR-induced mouse models. Also, most solid tumors show low Gpr162 expression, and higher expression is related to better prognosis in patients with lung adenocarcinoma, liver cancer, breast cancer, etc [1]. In pancreatic beta cells, Gpr162 is the receptor for Cocaine and amphetamine-regulated transcript (CART), mediating CART-induced insulin secretion and cytoskeletal arrangement [2].

In summary, Gpr162 has multiple functions in different biological processes. In cancer, it shows potential as a tumor suppressor and radiation sensitizer. In pancreatic beta cells, it is crucial for insulin-related functions. Studies on Gpr162, especially through model-based research, help understand its role in disease-related processes, providing insights for potential therapeutic strategies.