Serpinb2, also known as plasminogen activator inhibitor type 2 (PAI-2), is classically described as an inhibitor of extracellular urokinase plasminogen activator. However, its real biological role remains largely unknown. High-throughput studies suggest its functions in inflammation, autoimmune disorders, and carcinogenesis. Its expression can be acutely upregulated by various stimuli, including aryl hydrocarbon receptor ligands [1,2].

In Serpinb2-deficient MMTV-PyMT mice, tumor progression was delayed, and there was reduced tumor cell dissemination to lymph nodes. RNA-Seq data showed enriched genes related to inflammatory responses, with upregulated M1 and downregulated M2 macrophage marker genes. In vitro, SerpinB2 knockdown decreased the sphere formation and migration of MDA-MB-231 cells and suppressed protumorigenic M2 polarization of RAW264.7 cells [3].

SerpinB2 knockout mice subjected to kidney injury models showed enhanced kidney damage, fibrosis, and abnormal inflammatory cell infiltration. SerpinB2 knockout tubular cells had reduced CCL2 expression, and macrophages from these mice had reduced phagocytosis and enhanced migration [4].

Mice deficient in SerpinB2 expression had reduced tail bleeding times, suggesting a role in hemostasis [5].

In conclusion, Serpinb2 plays important roles in multiple biological processes. Through gene-knockout mouse models, its functions in tumor development, immune response in kidney injury, and hemostasis have been revealed. These findings contribute to understanding its roles in related disease areas such as breast cancer and kidney diseases, providing insights for potential therapeutic targets.