Ptprm, also known as Protein tyrosine phosphatase receptor type M, is a transmembrane receptor type tyrosine phosphatase. It plays crucial roles in various biological processes. In the nervous system, it is critical for synapse formation regulated by zinc ions, with zinc homeostasis being essential for normal brain functions [1]. It is also involved in cell adhesion via its extracellular domains and cell signaling via its cytoplasmic phosphatase domains [5].

In disease-related studies, loss-of-function experiments have shown its significance. In small intestinal neuroendocrine tumors (SI-NETs), reduced PTPRM expression was observed, and overexpression of PTPRM in SI-NET cell lines reduced cell growth, proliferation, and induced apoptosis, suggesting it as a candidate tumor suppressor gene [2]. In glioblastoma, FN1-induced PTPRM methylation promoted tumor development by activating STAT3 signalling [3]. In colorectal adenoma-carcinoma sequence, loss of PTPRM was associated with oncogenic cell growth, with its inactivation mainly due to loss of heterozygosity and promoter hypermethylation [4].

In conclusion, Ptprm is essential for synapse formation in the nervous system and plays important roles in multiple diseases. Loss-of-function studies in various cancer cell lines have revealed its potential as a tumor suppressor in some cancers, highlighting its significance in understanding disease mechanisms and potentially developing targeted therapies.