Prtn3, also known as proteinase 3, is an enzyme involved in various biological processes. It has been associated with multiple signaling pathways such as the PI3K/AKT and P38/ERK pathways, and plays important roles in immunoinflammatory responses, cancer progression, and metabolic processes [1].

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. It was found that Prtn3 in macrophages promotes the M2 polarization of tumor - associated macrophages, enhancing IL33/Treg - mediated tumor immunosuppression [2]. In mice, genetic elimination of Prtn3 led to spontaneous myeloid differentiation. Prtn3 interacts with the N - terminal of STAT3, promoting STAT3 ubiquitination and degradation, thus acting as a negative regulator of STAT3 - dependent myeloid differentiation. Deficiency of Prtn3 in primary AML blasts promotes their differentiation into functional neutrophils, improving overall survival rates for recipients [3].

In conclusion, Prtn3 is involved in regulating myeloid differentiation and plays a role in the tumor microenvironment, influencing tumor immunosuppression and cancer progression. The use of Prtn3 - knockout and conditional - knockout mouse models has provided valuable insights into its functions in cancer and leukemia, highlighting its potential as a therapeutic target in these disease areas.