Galectin-1: An important regulator in myeloid differentiation and acute myeloid leukemia as well as a promising prognostic indicator and therapeutic target.

Acute myeloid leukemia (AML) is an aggressive and heterogeneous hematological malignancy with a low survival probability and limited therapeutic options. Although galectin-1 (LGALS1) has been implicated in tumor cell survival and immune evasion in solid tumor, its role in AML is still unclear. In this study, we found that LGALS1 presents prominent upregulation in AML patients at both mRNA and protein levels compared with the control samples. Bioinformatics analysis indicated that high expression of LGALS1 is a significant unfavorable prognostic factor for overall survival in AML, correlating with adverse clinical and genetic features as well as immune cell infiltration. Depletion of LGALS1 in AML cells impeded cell proliferation, induced apoptosis and promoted myeloid differentiation. Treatment with OTX008, an LGALS1 inhibitor, markedly diminished the viability of primary malignant bone marrow cells from AML patients. Notably, LGALS1 expression was significantly reduced exclusively in AML-M5 patients after treatment, which may be due to its higher expression in AML-M5 subtype compared to other FAB subtypes. In summary, our findings indicate that LGALS1 could serve as an independent prognostic risk factor and a promising therapeutic target in AML, providing novel insights into AML pathogenesis and laying the foundation for the development of new therapeutic strategies.