Ptpn12, also known as protein tyrosine phosphatase non-receptor type 12, is a member of the proline -, glutamic acid -, serine-and threonine-rich (PEST) family of protein tyrosine phosphatases (PTPs) [1]. PTPs are crucial for regulating cell proliferation and differentiation in multicellular organisms. Ptpn12, in particular, is an important regulator of cell migration and adhesion by modulating multiple substrates. It is associated with pathways related to immune cell signaling, and has been considered a potential therapeutic target for diseases like cancer, diabetes, metabolic and autoimmune diseases [1].

In various cancers, Ptpn12 has been shown to act as a tumor suppressor gene. In laryngeal squamous cell carcinoma (LSCC), its down-regulation by miR-146b-3p affects the malignant progression, with over-expression of Ptpn12 inhibiting cell proliferation, migration, and invasion [2]. In nasopharyngeal carcinoma (NPC), Ptpn12 plasmid transfection suppressed cell proliferation and migration by negatively regulating EGFR [3]. In clear cell renal cell carcinoma (ccRCC), the expression of Ptpn12 protein and mRNA was significantly lower in cancer tissues compared to normal tissues, and was correlated with tumor diameter and clinical stage [4]. In esophageal squamous cell carcinoma (ESCC), lncRNA GATA2-AS1 upregulated Ptpn12 expression by competitively targeting miR-940, and GATA2-AS1 inhibited ESCC malignancy [5].

In conclusion, Ptpn12 is an important regulator in multiple biological processes, especially in cell migration, adhesion, and immune cell signaling. Its role as a tumor suppressor in various cancers, as revealed through in-vivo functional studies in different cancer models, highlights its potential as a molecular target for cancer diagnosis, prognosis analysis, and treatment [2,3,4,5].