Serpinf1, encoding pigment epithelium-derived factor (PEDF), is a member of the serpin family but lacks typical serine protease inhibitory activity. It has anti-tumor, anti-angiogenesis, anti-inflammation, nutrition and nerve protection functions, and is involved in fat metabolism [2].

In glioma, higher Serpinf1 expression correlates with poor overall survival. Knockdown of Serpinf1 suppresses glioma cell proliferation, invasion, migration and impairs the sphere formation of glioma stem cells. Bioinformatics analysis shows Notch signaling activation is associated with high Serpinf1 expression, and STAT1, CREM, and NR2F2 may participate in its transcriptional regulation [1].

In osteogenesis imperfecta type VI, Serpinf1 mutations lead to severe progressive deforming phenotypes. Homozygous in-frame deletions or insertions in Serpinf1 cause retention or degradation of PEDF within cellular compartments, interfering with its secretion [3].

In conclusion, Serpinf1 has diverse functions in different biological processes and diseases. In glioma, it may serve as a prognostic predictor and therapeutic target. In osteogenesis imperfecta type VI, its mutations disrupt normal PEDF secretion and cause bone-related phenotypes. These findings from functional studies help understand the role of Serpinf1 in disease development and potentially guide treatment strategies.