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首页> 外文期刊>Molecular and Cellular Biology >The Activated Notch1 Receptor Cooperates with α-Enolase and MBP-1 in Modulating c-myc Activity
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The Activated Notch1 Receptor Cooperates with α-Enolase and MBP-1 in Modulating c-myc Activity

机译：激活的Notch1受体与α-烯醇酶和MBP-1协同调节c-myc活性。

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The Notch signal pathway plays multifaceted roles to promote or suppress tumorigenesis. The Notch1 receptor intracellular domain (N1IC), the activated form of the Notch1 receptor, activates the c-myc proto-oncogene. The complex of N1IC and transcription factor YY1 binds to the human c-myc promoter to enhance c-myc expression in a CBF1-independent manner. Here we demonstrated that N1IC interacted with the c-Myc-regulating proteins α-enolase and c-myc promoter binding protein 1 (MBP-1). Both α-enolase and MBP-1 suppressed the N1IC-enhanced activity of the c-myc promoter in a CBF1-independent manner. The YY1 response element in front of the P2 c-myc promoter was essential and sufficient for the modulation of c-myc by N1IC and α-enolase or MBP-1. Furthermore, N1IC, YY1, and α-enolase or MBP-1 but not CBF1 bound to the c-myc promoter through associating with the YY1 response element. Hemin-induced erythroid differentiation was suppressed by N1IC in K562 cells. This suppression was relieved by the expression of α-enolase and MBP-1. In addition, both α-enolase and MBP-1 suppressed the N1IC-enhanced colony-forming ability through c-myc. These results indicate that the activated Notch1 receptor and α-enolase or MBP-1 cooperate in controlling c-myc expression through binding the YY1 response element of the c-myc promoter to regulate tumorigenesis.
机译：Notch信号通路在促进或抑制肿瘤发生中起着多方面的作用。 Notch1受体的细胞内结构域（N1IC）是Notch1受体的激活形式，它激活c- myc 原癌基因。 N1IC和转录因子YY1的复合物与人c- myc 启动子结合，以CBF1独立的方式增强c- myc 表达。在这里，我们证明了N1IC与c-Myc调节蛋白α-烯醇酶和c- myc 启动子结合蛋白1（MBP-1）相互作用。 α-烯醇酶和MBP-1均以不依赖CBF1的方式抑制c- myc 启动子的N1IC增强活性。 P2 c- myc 启动子前面的YY1反应元件对于N1IC和α-烯醇酶或MBP-1调节c- myc 至关重要。此外，N1IC，YY1和α-烯醇酶或MBP-1而非CBF1通过与YY1反应元件结合而与c- myc 启动子结合。 N1IC在K562细胞中抑制了血红素诱导的类红细胞分化。通过α-烯醇酶和MBP-1的表达减轻了这种抑制。另外，α-烯醇酶和MBP-1均通过c- myc 抑制N1IC增强的菌落形成能力。这些结果表明，活化的Notch1受体和α-烯醇酶或MBP-1通过将c- myc 启动子的YY1反应元件结合到c- myc 上，共同控制c- myc 的表达。调节肿瘤发生。

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