Ptprs, also known as protein tyrosine phosphatase receptor sigma, is a receptor-type protein tyrosine phosphatase. It plays roles in multiple biological processes by regulating cell migration, invasion, and the activation of various signaling pathways such as the RAS-ERK pathway. It is involved in maintaining synaptic integrity and is related to the epithelial-mesenchymal transition (EMT) process [1-4, 6, 8].

In NF1-related plexiform neurofibromas, reduced PTPRS expression promotes the EMT of Schwann cells, and this is associated with tumor recurrence. PTPRS knockdown can promote EGFR expression and phosphorylation, and restoring the disrupted EMT processes by EGFR knockdown or using an EGFR inhibitor [1].

In Alzheimer's disease, the PTPRS rs10415488 variant C shows neuroprotective features against early tau pathology and synaptic degeneration, with a sexual dimorphism observed where male carriers have a delayed disease onset [2,4].

In colorectal cancer, PTPRS mutations can reduce its phosphatase activity, increasing ERK activation and downstream signaling [3,5].

In glioblastoma, loss of PTPRS leads to potent metastatic capability and resistance to temozolomide [6].

In conclusion, Ptprs is crucial in regulating cell behavior and signaling pathways. Studies using models with PTPRS alterations, like knockdown or mutation models, have revealed its significant roles in diseases such as neurofibromas, Alzheimer's disease, colorectal cancer, and glioblastoma, highlighting its potential as a therapeutic target in these disease areas.