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Role of NSD1 in H_2O_2-induced GSTM3 suppression

机译：NSD1在H_2O_2诱导的GSTM3抑制中的作用

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摘要

Nuclear receptor-binding SET domain-containing protein 1 (NSD1) has been proved to act as a histone methyltransferase and a transcription co-factor to regulate gene expression. However, the role of NSD1 in oxidative stress remains poorly understood. In the present study, we focused on the NSD1 regulation of antioxidant enzyme gene glutathione S-transferase M3 (GSTM3) expression in response to oxidative stress. H_2O_2 treatment caused the decrease of both NSD1 and GSTM3 expression, and the depletion of NSD1 expression by specific siRNA reversed the H_2O_2-reduced GSTM3 expression. Furthermore,we investigated NSD1modulating the transcription of GSTM3 promoter with -63A/C polymorphism closed to TATA box in response to H_2O_2 by luciferase and in vitro or in vivo DNA-protein binding assays. The promoter activity of GSTM3 with -63A was higher than -63C, and was increased or decreased by the overexpression or depletion of NSD1, but -63C was not influenced. H_2O_2 repressed the promoter activity of GSTM3 with -63A more than -63C, and the depletion of NSD1 expressionweakenedH_2O_2 inhibition on the-63A promoter, but augmented H_2O_2 inhibition on the-63C promoter. In addition, NSD1 interacted with RNAPII and bound to GSTM3-63A/C TATA box, with higher binding affinity to -63A than to -63C. These data indicated that NSD1 implicated in H_2O_2-induced oxidative stress, and H_2O_2-induced NSD1 suppression resulted in the decrease of GSTM3 expression through the -63A/C TATA box.
机译：含核受体结合SET域的蛋白质1（NSD1）已被证明可作为组蛋白甲基转移酶和转录辅因子来调节基因表达。但是，NSD1在氧化应激中的作用仍然知之甚少。在本研究中，我们集中于NSD1调节抗氧化酶基因谷胱甘肽S-转移酶M3（GSTM3）表达以响应氧化应激。 H_2O_2处理导致NSD1和GSTM3表达均降低，而特异性siRNA耗尽NSD1表达则逆转了H_2O_2降低的GSTM3表达。此外，我们通过荧光素酶和体外或体内DNA-蛋白质结合试验研究了NSD1调节具有-63A / C多态性的GSTM3启动子的转录，该多态性接近于TATA盒，响应H_2O_2。具有-63A的GSTM3的启动子活性高于-63C，并且由于NSD1的过表达或耗尽而增加或降低，但-63C不受影响。 H_2O_2比-63C高-63A抑制GSTM3的启动子活性，NSD1表达的耗竭使H_2O_2对-63A启动子的抑制作用减弱，但对H_2O_2对-63C启动子的抑制作用增强。此外，NSD1与RNAPII相互作用并与GSTM3-63A / C TATA盒结合，与-63A的结合亲和力高于对-63C的结合亲和力。这些数据表明，NSD1与H_2O_2诱导的氧化应激有关，而H_2O_2诱导的NSD1抑制则通过-63A / C TATA框导致GSTM3表达降低。

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