SUMO specific peptidase 1 decreases after induction treatment, and its reduction predicts lower disease risk, better treatment response, longer survival of acute myeloid leukemia.

Small ubiquitin-related modifier-specific peptidase 1 (SENP1) takes part in the pathogenesis and progression of hematological malignancies, while its clinical role in acute myeloid leukemia (AML) is unclear. This study aimed to explore the potential of SENP1 to serve as a biomarker reflecting disease risk, treatment response, and survival of AML. A total of 110 AML patients, 30 disease controls (DCs), and 30 healthy controls (HCs) were included. SENP1 in bone marrow samples was detected by RT-qPCR. SENP1 was the top in AML patients (median (interquartile range (IQR)): 2.429 (1.854-3.772)), the second top in DCs (median (IQR): 1.587 (1.023-2.217)), and the lowest in HCs (median (IQR): 0.992 (0.806-1.702)) ( < 0.001). In AML patients, SENP1 was positively associated with white blood cells ( = 0.210,  = 0.028) and bone marrow blasts ( = 0.212,  = 0.026) but negatively linked to Inv(16) or t(16;16) presence ( = 0.040). Furthermore, SENP1 was decreased post-treatment vs. at baseline (before induction treatment) in total AML patients ( < 0.001), and in patients with CR ( < 0.001), but not in patients with non-CR ( = 0.055). Additionally, SENP1 at baseline slightly ( = 0.050) but SENP1 post-treatment dramatically ( < 0.001) decreased in patients with CR compared to those with non-CR. Notably, low SENP1 at baseline was related to prolonged EFS ( = 0.007) and OS ( = 0.039); meanwhile, declined SENP1 post-induction treatment showed a more predominant linkage with satisfied EFS ( < 0.001) and OS ( < 0.001). SENP1 is decreased after induction therapy, whose reduction is related to low disease risk, favorable treatment response, and prolonged survival of AML.