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 β-catenin expression, a change that led to inactivation of Wnt/β-catenin pathway. Notably, restoration of β-catenin expression partially reversed SOX30-mediated tumor suppressive effect in AML cells. In an AML-derived 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/β-catenin axis in the progression of AML.

中文翻译：

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SOX30通过灭活Wnt /β-catenin信号传导赋予急性髓性白血病肿瘤抑制作用。

最近的研究表明，SRY相关的高迁移率族盒30（SOX30）作为多种肿瘤类型的候选肿瘤促进剂或肿瘤抑制剂。然而，尚未充分研究SOX30在急性髓细胞性白血病（AML）中的详细作用。本研究旨在调查SOX30与AML的详细相关性。我们的研究数据表明SOX30的表达在AML细胞中显着下调，这是与其高甲基化有关的一种模式。SOX30的过表达导致AML细胞增殖和集落形成明显减少，但它促进了AML细胞凋亡。相比之下，小干扰RNA（siRNA）介导的基因沉默导致的SOX30消耗却相反。此外，SOX30过表达显着降低了β-catenin表达，这一改变导致Wnt /β-catenin途径失活。值得注意的是 β-catenin表达的恢复可部分逆转SOX30介导的AML细胞抑癌作用。在AML衍生的小鼠异种移植模型中，SOX30的过表达显着延迟了体内肿瘤的生长。总体而言，该研究的这些数据表明SOX30在AML中具有肿瘤抑制作用，并突出了SOX30 / Wnt /β-catenin轴在AML进展中的关键作用。