Gfra3, also known as GDNF family receptor alpha 3, is a receptor for artemin (ARTN), a glial cell line-derived neurotrophic factor (GDNF) [2]. It has been associated with multiple biological processes and disease conditions.

In the context of early embryonic development, the artemin-GFRA3 signaling system may play an autocrine/paracrine role in regulating development and apoptosis, possibly involving the MAP kinase signaling pathway [5].

In gastric cancer, high expression of GFRA3 is associated with poor prognosis, and the ARTN-GFRA3 axis can induce epithelial-mesenchymal transition phenotypes, migration, and invasion of gastric cancer cells via KRAS signaling [2]. In lung adenocarcinoma, the expression of GFRA3 is upregulated after cuproptosis is induced, and the deficiency of GFRA3 can facilitate cuproptosis induced by elesclomol-CuCL2 [3]. In hepatocellular cancer, GFRA3 is significantly correlated with clinical prognosis, stage, immune infiltration, immune response, and vital signaling pathways [4]. Also, in the study of neuropathic pain, Gfra3 was found to be expressed in one of the SNI-induced neuronal clusters in mouse dorsal root ganglia after nerve injury, providing insights into the development of neuropathic pain [1].

In conclusion, GFRA3 plays crucial roles in multiple biological processes and disease conditions such as cancer development and neuropathic pain. Studies on GFRA3, especially through in vivo models like mouse models in relevant disease areas, help to understand its functions in different physiological and pathological states, potentially providing new directions for disease treatment.