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Ribosomal RACK1 promotes proliferation of neuroblastoma cells independently of global translation upregulation.
Cellular Signalling ( IF 4.8 ) Pub Date : 2018-10-01 , DOI: 10.1016/j.cellsig.2018.09.020
Nicla Romano 1 , Matteo Veronese 1 , Nicola Manfrini 1 , Lello Zolla 2 , Marcello Ceci 1
Affiliation  

Neuroblastoma is the most frequent solid tumor among those diagnosed during infancy and like most tumors, it is characterized by elevated rates of cell proliferation, migration and invasion. RACK1 is among the top 10 genes identified for unfavorable prognosis at 5 years in neuroblastoma cases and its depletion negatively affects proliferation, invasion and migration. Here, we show that the ribosomal localization of RACK1 modulates the proliferation of SH-SY5Y neuroblastoma cells by regulating the expression of cell cycle genes, such as Cyclin D1, D3 and B1 independently of global translation increase. Ribosomal RACK1 is not involved in general protein synthesis, which is instead dependent on total RACK1 and PKC but independent from mTOR. Thus, ribosomal RACK1 may represent a new target to develop more efficient therapies for neuroblastoma treatment.

中文翻译:

核糖体RACK1促进神经母细胞瘤细胞的增殖,独立于整体翻译上调。

神经母细胞瘤是婴儿期诊断出的最常见的实体瘤,与大多数肿瘤一样,它的特征在于细胞增殖,迁移和侵袭的速率增加。RACK1是在神经母细胞瘤病例中被鉴定为5年不良预后的前10个基因之一,其耗竭对增殖,侵袭和迁移产生负面影响。在这里,我们显示RACK1的核糖体定位通过调节细胞周期基因(如细胞周期蛋白D1,D3和B1)的表达而独立于整体翻译的增加,从而调节SH-SY5Y神经母细胞瘤细胞的增殖。核糖体RACK1不参与一般的蛋白质合成,而是依赖于总RACK1和PKC,但不依赖于mTOR。因此,
更新日期:2018-10-01
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