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| Content Provider | World Health Organization (WHO)-Global Index Medicus |
|---|---|
| Author | Kawamura, Miyuki Watanabe, Yoshinori Sugimura, Haruhiko Honda, Takashi Tanno, Yuji Susumu, Hiroaki |
| Description | Author Affiliation: Tanno Y ( Laboratory of Chromosome Dynamics, Institute of Molecular and Cellular Biosciences, University of Tokyo, Yayoi, Tokyo 113-0032, Japan.); Susumu H ( Laboratory of Chromosome Dynamics, Institute of Molecular and Cellular Biosciences, University of Tokyo, Yayoi, Tokyo 113-0032, Japan. Department of Biological Sciences, Graduate School of Science, University of Tokyo, Yayoi, Tokyo 113-0032, Japan.); Kawamura M ( Laboratory of Chromosome Dynamics, Institute of Molecular and Cellular Biosciences, University of Tokyo, Yayoi, Tokyo 113-0032, Japan. Department of Biological Sciences, Graduate School of Science, University of Tokyo, Yayoi, Tokyo 113-0032, Japan.); Sugimura H ( First Department of Pathology, Hamamatsu University School of Medicine, Hamamatsu, Shizuoka 431-3192, Japan.); Honda T ( Laboratory of Chromosome Dynamics, Institute of Molecular and Cellular Biosciences, University of Tokyo, Yayoi, Tokyo 113-0032, Japan.); Watanabe Y ( Laboratory of Chromosome Dynamics, Institute of Molecular and Cellular Biosciences, University of Tokyo, Yayoi, Tokyo 113-0032, Japan. Department of Biological Sciences, Graduate School of Science, University of Tokyo, Yayoi, Tokyo 113-0032, Japan. ywatanab@iam.u-tokyo.ac.jp.) |
| Abstract | Chromosomal instability (CIN) is a major trait of cancer cells and a potent driver of tumor progression. However, the molecular mechanisms underlying CIN still remain elusive. We found that a number of CIN(+) cell lines have impairments in the integrity of the conserved inner centromere-shugoshin (ICS) network, which coordinates sister chromatid cohesion and kinetochore-microtubule attachment. These defects are caused mostly by the loss of histone H3 lysine 9 trimethylation at centromeres and sometimes by a reduction in chromatin-associated cohesin; both pathways separately sustain centromeric shugoshin stability. Artificial restoration of the ICS network suppresses chromosome segregation errors in a wide range of CIN(+) cells, including RB- and BRCA1-deficient cells. Thus, dysfunction of the ICS network might be a key mechanism underlying CIN in human tumorigenesis. |
| ISSN | 00368075 |
| Issue Number | 6253 |
| Volume Number | 349 |
| e-ISSN | 10959203 |
| Journal | Science |
| Language | English |
| Publisher | American Association for the Advancement of Science (United States) |
| Publisher Date | 2015-09-11 |
| Publisher Place | United States |
| Access Restriction | One Nation One Subscription (ONOS) |
| Subject Keyword | Carcinogenesis Metabolism Cell Cycle Proteins Centromere Chromosomal Instability Chromosome Segregation BRCA1 Protein Genetics Chromatids Chromatin Chromosomal Proteins, Non-Histone HeLa Cells Histones Humans Kinetochores Lysine Methylation Microtubules Retinoblastoma Protein Journal Article Research Support, Non-U.S. Gov't Multidisciplinary |
| Content Type | Text |
| Resource Type | Article |
| Subject | History and Philosophy of Science |
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