SOX30 confers a tumor suppressive effect in acute myeloid leukemia through inactivation of Wnt/β-catenin signaling

Recent studies suggested SRY-related high mobility group box 30 (SOX30) as a candidate tumor-promoter or tumor-inhibitor in multiple tumor types. Yet, the detailed role of SOX30 in acute myeloid leukemia (AML) has not been well studied. The present research was designed to investigate the detailed relevance of SOX30 in AML. The data of our study indicated that SOX30 expression was markedly downregulated in AML cells, a pattern associated with its hypermethylation. SOX30 overexpression caused a marked reduction in AML cell proliferation and colony formation, but it promoted AML cell apoptosis. By contrast, SOX30 depletion by small interfering RNA (siRNA)-mediated gene silencing had the opposite effect. Moreover, SOX30 overexpression markedly decreased beta-catenin expression, a change that led to inactivation of Wnt/beta-catenin pathway. Notably, restoration of beta-catenin expression partially reversed SOX30-mediated tumor suppressive effect in AML cells. In an AMLderived mouse xenograft model, SOX30 overexpression remarkably retarded the tumor growth in vivo. Overall, these data of the study suggest a tumor-inhibition role of SOX30 in AML, and highlight a key role of SOX30/Wnt/beta-catenin axis in the progression of AML.