电离辐射对胶质母细胞瘤细胞c-Myc和NBS1的调控

Paulo Matheus Guerra Rodrigues , Roberto Salomon de Souza , Helena Lobo Borges , Rodrigo Alves Portela Martins
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引用次数: 1

摘要

胶质母细胞瘤是最常见的原发性脑肿瘤,预后最差。这些肿瘤的放射耐药是更好的治疗和管理的障碍。细胞对电离辐射(IR)的反应取决于多种分子机制,包括DNA损伤反应基因对致癌基因的转录。以往的研究表明,胶质瘤干细胞的放射耐药可能与c- myc依赖性上调NBS1有关。本研究的目的是评估IR和其他dna损伤剂是否在胶质母细胞瘤细胞系中共同调节c-Myc和NBS1。我们发现,在特定的胶质母细胞瘤细胞系中,IR会下调c-Myc蛋白水平,而NBS1蛋白含量不会因基因毒性药物而改变。此外,ir诱导的c-Myc蛋白含量下调与细胞活力降低无关。这些发现表明,在遗传毒性应激背景下,c-Myc和NBS1之间的功能关系可能是遗传背景特异性的。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Regulation of c-Myc and NBS1 by ionizing radiation in glioblastoma cells

Glioblastoma is the most common primary brain tumor presenting the worst prognostic. Radioresistance of these tumors is barrier to better treatment and management. Cellular response to ionizing radiation (IR) depends on various molecular mechanisms, including transcription of DNA damage response genes in response to oncogenes. Previous studies suggested that the radioresistance of glioma stem cells would be associated with c-Myc-dependent upregulation of NBS1. The purpose of this study was to evaluate whether IR and other DNA-damaging agents co-regulate c-Myc and NBS1 in glioblastoma cell lines. We found that c-Myc protein level is downregulated by IR in specific glioblastoma cell lines, while NBS1 protein content was not altered in response to genotoxic agents. Additionally, IR-induced downregulation of c-Myc protein content had no correlation with decreased cell viability. These findings indicate that the functional relationship between c-Myc and NBS1 in the context of genotoxic stress may be genetic background-specific.

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