Adgrd1, also known as GPR133, is an adhesion G protein-coupled receptor. It signals through Gαs/cyclic AMP (cAMP) pathway and is crucial for multiple biological functions. It has been associated with processes like cancer growth, immune response-related regulation, and embryo transit in mice, highlighting its overall biological importance. Genetic models, such as knockout (KO) mouse models, can be valuable for further studying its functions [2,3,4,5].

In non-small-cell lung cancer (NSCLC), Adgrd1 expression is decreased and may predict prognosis. It also shows significant correlations with tumor mutational burden (TMB), microsatellite instability (MSI), and immune cell infiltration levels in lung adenocarcinoma and squamous cell carcinoma. The most promising upstream regulation pathways involve miR-142-5p, miR-93-5p, and miR-17-5p [1]. In glioblastoma, Adgrd1 is necessary for tumor growth. Genetic inhibition of Adgrd1 in glioblastoma cells reduces the prevalence of cancer stem-like cells, tumor cell proliferation, and tumorsphere formation in vitro, and decreases tumor xenograft formation in mouse brains [4]. In female mice, Adgrd1-deficient models are sterile as the gene is essential for embryo transit. It is expressed on the oviductal epithelium and regulates oviductal fluid flow [5].

In conclusion, Adgrd1 is essential for embryo transit in mice and plays significant roles in cancer, especially in glioblastoma growth and NSCLC prognosis. The use of Adgrd1 KO mouse models has been instrumental in revealing its functions in these specific biological processes and disease conditions, providing insights into potential therapeutic targets in cancer and understanding of embryo-related disorders [1,4,5].