NIPA1 depletion in tumor-associated macrophages via IGFBP2/EGFR attenuates acute myeloid leukemia progression and chemoresistance.

ABSTRACT: Acute myeloid leukemia (AML) is an aggressive and heterogenous malignancy, with unsatisfactory clinical outcomes even with very intensive treatment strategies. Previous research has revealed that Prader-Willi/Angelman syndrome 1 (NIPA1) is highly expressed in patients with AML and is negatively correlated with overall survival. However, studies on the molecular mechanism of NIPA1 in AML remain limited. To explore the role of NIPA1and its molecular mechanism in AML, we discovered through cellular experiments that NIPA1 was upregulated in M2 macrophages. NIPA1 knockdown inhibited M2 macrophage polarization and the survival of AML cells. In animal experiments, we also found that NIPA1 depletion restricted tumor growth in mice with AML. Further studies indicated that NIPA1 knockdown inhibited

SUBMITTER: Tang S 

PROVIDER: S-EPMC12619713 | biostudies-literature | 2025 Oct

REPOSITORIES: biostudies-literature