title: Molecular profiling of MPS1 gene silencing in U251 glioma cell line.
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 glioblastomas (GBM)[1, 2]. Monopolar spindle 1 (MPS1), is an essential spindle assembly checkpoint kinase that is overexpressed in several human cancers [3-5]. In our previous publication, we have shown the role of MPS1 kinase in DNA repair and enhanced radiosensitivity in GBM[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 hours after transfection. The raw data of this study is deposited in Gene Expression Omnibus under the accession number GSE57091.
authors.affiliation: Radiation Oncology Branch, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892.
authors.forename: Uma
authors.initials: U
authors.lastname: Shankavaram
authors.affiliation: Radiation Oncology Branch, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892.
authors.forename: Uday Bhanu
authors.initials: UB
authors.lastname: Maachani
authors.affiliation: Radiation Oncology Branch, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892.
authors.forename: Shuping
authors.initials: S
authors.lastname: Zhao
authors.affiliation: Radiation Oncology Branch, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892.
authors.forename: Kevin
authors.initials: K
authors.lastname: Camphausen
authors.affiliation: Radiation Oncology Branch, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892.
authors.forename: Anita
authors.initials: A
authors.lastname: Tandle