MOSPD1, Motile Sperm Domain-Containing Protein 1, is part of a gene family including Mospd2 and Mospd3, characterized by the major sperm protein domain and two transmembrane domains. It is located in the endoplasmic reticulum and Golgi apparatus, and can localize to the nucleus under certain conditions [2]. MOSPD1 may play roles in membrane contact sites as it can interact with FFAT-related FFNT motifs [4,5,7]. It is involved in multiple biological processes, and its dysregulation is associated with various diseases.

In breast cancer, MOSPD1 expression is significantly higher in cancer samples than normal tissues, correlating with poor clinical outcomes. MOSPD1 suppression inhibits tumor growth, while overexpression accelerates it. Silencing MOSPD1 also enhances breast cancer cell sensitivity to anti-PD-L1 therapy and decreases Th2 cell activity [1].

In gastric cancer, MOSPD1 promotes cancer progression by facilitating fatty acid metabolism through activating the MAPK pathway. MOSPD1 knockdown decreases the proliferation, migration, and invasion of gastric cancer cells [3].

In mesenchymal stem cells (MSCs), MOSPD1-null embryonic stem cells are deficient in differentiating into several cell lineages including osteoblasts, adipocytes, and hematopoietic progenitors, and the growth rate of MSC-like cells derived from MOSPD1-null ESCs is significantly impaired [6].

In colorectal cancer, MOSPD1 is upregulated by the Wnt/β-catenin signaling pathway [8].

In conclusion, MOSPD1 is crucial in multiple biological processes such as cell differentiation and proliferation. Its dysregulation significantly impacts the development and progression of various cancers, including breast, gastric, and colorectal cancer. The use of gene knockout models in mice has been instrumental in revealing these functions, providing potential therapeutic targets for these diseases.