Small ubiquitin-like modifier (SUMO) family proteins regulate target-protein functions by post-translational modification. However, a potent and selective inhibitor targeting the SUMO pathway has been lacking. Here we describe ML-792, a mechanism-based SUMO-activating enzyme (SAE) inhibitor with nanomolar potency in cellular assays. ML-792 selectively blocks SAE enzyme activity and total SUMOylation, thus decreasing cancer cell proliferation. Moreover, we found that induction of the MYC oncogene increased the ML-792-mediated viability effect in cancer cells, thus indicating a potential application of SAE inhibitors in treating MYC-amplified tumors. Using ML-792, we further explored the critical roles of SUMOylation in mitotic progression and chromosome segregation. Furthermore, expression of an SAE catalytic-subunit (UBA2) S95N M97T mutant rescued SUMOylation loss and the mitotic defect induced by ML-792, thus confirming the selectivity of ML-792. As a potent and selective SAE inhibitor, ML-792 provides rapid loss of endogenously SUMOylated proteins, thereby facilitating novel insights into SUMO biology.

译文

:小泛素样修饰子(SUMO)家族蛋白通过翻译后修饰来调节靶蛋白的功能。然而,一直缺乏靶向SUMO途径的有效和选择性抑制剂。在这里,我们描述ML-792,这是一种基于机制的SUMO活化酶(SAE)抑制剂,在细胞测定中具有纳摩尔浓度。 ML-792有选择地阻断SAE酶的活性和总SUMOylation,从而减少癌细胞的增殖。此外,我们发现MYC癌基因的诱导增加了癌细胞中ML-792介导的生存能力,从而表明SAE抑制剂在治疗MYC扩增的肿瘤中的潜在应用。使用ML-792,我们进一步探索了SUMOylation在有丝分裂进程和染色体分离中的关键作用。此外,SAE催化亚基(UBA2)S95N M97T突变体的表达挽救了SUMOylation损失和ML-792诱导的有丝分裂缺陷,从而证实了ML-792的选择性。作为一种有效且选择性的SAE抑制剂,ML-792可快速损失内源性SUMO酰化的蛋白质,从而促进对SUMO生物学的新见解。

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