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Molecular profiling of {MPS1} gene silencing in {U251} glioma cell line

机译:{U251}胶质瘤细胞株中{MPS1}基因沉默的分子概况

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Abstract Aneuploidy has been recognized as a common characteristic of cancers. Aneuploidy frequently results from errors of the mitotic checkpoint, the major cell cycle control mechanism that acts to prevent chromosome missegregation. Mutation of the genes that control chromosome segregation during mitosis may explain the high rate of chromosomal instability and aneuploidy, a characteristic of most solid tumors, including glioblastoma (GBM) (Gordon et al., 2012 [1]; Singh et al., 2012 [2]). Monopolar spindle 1 (MPS1) is an essential spindle assembly checkpoint kinase that is overexpressed in several human cancers (Kilpinen et al., 2010 [3]; Mills et al., 1992 [4]; Yuan et al., 2006 [5]). In our previous publication, we have shown the role of {MPS1} kinase in {DNA} repair and enhanced radiosensitivity in {GBM} (Maachani et al., 2015 [6]). Here, we provide methodological and analytical details of that study, to compare mRNA expression profile of siMPS1-silenced {U251} cells with untransfected control, and siRNA control (siNeg) at 6, 24, and 48 h after transfection. The raw data of this study is deposited in Gene Expression Omnibus under the accession number GSE57091.
机译:摘要非整倍性已被认为是癌症的共同特征。非整倍性通常是由有丝分裂检查点的错误引起的,有丝分裂检查点是防止染色体错聚的主要细胞周期控制机制。控制有丝分裂期间染色体分离的基因突变可能解释了染色体不稳定和非整倍性的高发生率,这是包括胶质母细胞瘤(GBM)在内的大多数实体瘤的特征(Gordon等,2012 [1]; Singh等,2012 [2])。单极纺锤体1(MPS1)是必需的纺锤体装配检查点激酶,在几种人类癌症中均过表达(Kilpinen等,2010 [3]; Mills等,1992 [4]; Yuan等,2006 [5] )。在我们以前的出版物中,我们显示了{MPS1}激酶在{DNA}修复中的作用和{GBM}中增强的放射敏感性(Maachani等人,2015 [6])。在这里,我们提供了该研究的方法和分析细节,以比较未转染对照和转染后6、24和48小时的siMPS1沉默的{U251}细胞与siRNA对照(siNeg)的mRNA表达谱。这项研究的原始数据以登录号GSE57091保存在Gene Expression Omnibus中。

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