Rasd2, encoding a Ras-related GTP-binding protein, is involved in multiple biological functions. It is associated with psychiatric disorders and has been shown to be expressed in various tissues like skin [1,4]. The Rhes/RASD2 GTPase complex is part of dopamine D1/D2 receptor-mediated signaling [6].

In UVM, silencing Rasd2 dampened cell growth, migration, and invasion both in vitro and in vivo, suggesting it promotes UVM development and metastasis via enhancing glycolysis [1]. In ovariectomized mice, Rasd2 overexpression in the hippocampus alleviated depression-like behaviors, and 9-hour fasting had antidepressant-like effects by upregulating Rasd2 and related proteins, blocked by DRD2 antagonists [2]. Also, in mice, 5-day unpredictable mild stress reduced Rasd2 expression, and its overexpression in the NAcc core alleviated stress-induced depression-like behaviors [3]. In thyroid cancer, genetic silencing of Rasd2 impaired malignant phenotypes, and miRNA-485-5p was identified as a negative regulator of Rasd2 [5].

In summary, Rasd2 plays significant roles in multiple disease conditions. In cancer, such as UVM and thyroid cancer, it promotes tumor-related processes. In psychiatric-related models, it is involved in depression-like behaviors. Gene knockout or knockdown models in mice have been crucial in revealing these functions, providing insights into potential therapeutic strategies for these diseases.