Castor1, short for cytosolic arginine sensor for the mTOR complex 1 (mTORC1) subunit 1, is an important arginine sensor in the mTORC1 pathway [2]. The mTORC1 pathway is a central controller of cell proliferation in response to growth factors and nutrients, and Castor1 plays a role in this regulation, with its function having implications for various biological processes and diseases [3].

In microglia, Castor1 expression was decreased when treated with lipopolysaccharides (LPS) and interferon (IFN)-γ. Overexpression of Castor1 inhibited M1 polarization and promoted M2 polarization by inhibiting the mTOR signaling pathway, suggesting its potential as a target for central nervous system-related diseases [1]. In breast cancer, the E3 ubiquitin ligase RNF167 promotes CASTOR1 degradation, activating mTORC1 and promoting breast cancer progression [3]. In lung adenocarcinoma, Castor1 expression was reduced in tumor tissues compared to normal lung tissues. Its overexpression suppressed cellular proliferation, migration, and invasion, and low Castor1 expression was associated with a worse 5-year survival rate, indicating it might be a therapeutic target or prognostic marker [6]. In male patients with KRAS-mutated lung adenocarcinoma, elevated pCASTOR1 scores predicted poorer overall and relapse-free survival [4]. In mammary epithelial cells, heat stress increased CASTOR1 expression, and downregulation of CASTOR1 inhibited heat-stress-induced apoptosis and promoted milk component synthesis [5].

In conclusion, Castor1 is a crucial regulator in the mTORC1 pathway, with its function influencing microglial polarization, cancer progression, and responses to stress in various cell types. Studies on Castor1, including those using potential KO/CKO mouse models (although not explicitly detailed in the given references), could further our understanding of its role in central nervous system-related diseases, cancer, and other biological processes, potentially leading to new therapeutic strategies.