SOSTDC1 acts as a tumor inhibitor in acute myeloid leukemia by downregulating the Wnt/β-catenin pathway

Sclerostin domain-containing 1 (SOSTDC1) has been documented as a key tumor-associated protein that is differentially expressed in multiple malignancies. However, the function of SOSTDC1 in acute myeloid leukemia (AML) is unexplored. The goal of this work was to assess the possible role of SOSTDC1 in AML. Our data showed decreased SOSTDC1 level in bone marrow from AML patients, and patients with low levels of SOSTDC1 had a reduced survival rate. SOSTC1 upregulation restrained the proliferative ability and promoted the apoptotic rate of AML cells. SOSTDC1 suppressed the activation of the Wnt/beta-catenin pathway in AML cells. Reactivation of the Wnt/beta-catenin pathway reversed SOSTDC1-mediated antitumor effects. SOSTDC1 upregulation weakened the tumorigenicity of AML cells in vivo. Collectively, our work demonstrates that SOSTDC1 has a tumor-inhibiting role in AML via downregulation of the Wnt/beta-catenin pathway. This work underscores a key function for the SOSTDC1/Wnt/beta-catenin pathway in AML.