Prtn3, also known as proteinase 3, is a protein-encoding gene. Proteinase 3 is a serine protease that has been implicated in various biological processes and diseases. It is involved in immune-inflammatory responses, cancer-related pathways such as the PI3K/AKT and P38/ERK signaling pathways, and may play a role in collagen degradation in the tumor microenvironment [1,2,7].

In a myeloid cells-specific Prtn3-knockout mouse model, Prtn3 deficiency in macrophages was shown to remold the immunosuppressive tumor microenvironment and suppress tumor growth in lung adenocarcinoma. This indicated that Prtn3 in macrophages acts as a key immunoregulator, enhancing IL33/Treg-mediated tumor immunosuppression by promoting M2 polarization of tumor-associated macrophages [2]. In another study, genetic elimination of Prtn3 in mice led to spontaneous myeloid differentiation. Mechanistically, Prtn3 was found to interact with the N-terminal of STAT3, promoting STAT3 ubiquitination and degradation, thus negatively regulating STAT3-dependent myeloid differentiation. Deficiency of Prtn3 in primary AML blasts promoted their differentiation into functional neutrophils, improving overall survival rates for recipients [5].

In conclusion, Prtn3 plays crucial roles in tumor-related immunosuppression and myeloid differentiation. Studies using Prtn3 knockout mouse models have provided valuable insights into its functions in lung adenocarcinoma and leukemia, highlighting its potential as a therapeutic target in these disease areas. Additionally, Prtn3 may be involved in other cancer-related processes and could potentially serve as a biomarker in diseases like early gastric cancer, esophageal cancer, and pancreatic cancer, as well as in sepsis diagnosis and periprosthetic joint infection [1,2,3,4,6,7,8].