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Suppression of polyploidy by the BRCA2 protein.

Abstract
Mounting evidence implicates BRCA2 not only in maintenance of genome integrity but also in cell-cycle checkpoints. However, the contribution of BRCA2 in the checkpoints is still far from being understood. Here, we demonstrate that breast cancer cells MX-1 are unable to maintain genome integrity, which results in gross polyploidization. We generated MX-1 clones, stably expressing BRCA2, and found that BRCA2 acts to suppress polyploidy. Compared with MX-1, the ectopically BRCA2-expressing cells had different intracellular levels of Aurora A, Aurora B, p21, E2F-1, and pRb, suggesting a BRCA2-mediated suppression of polyploidy via stabilization of the checkpoint proteins levels.
AuthorsEvgeny Sagulenko, Larissa Savelyeva, Volker Ehemann, Vitaliya Sagulenko, Wera Hofmann, Katrin Arnold, Andreas Claas, Siegfried Scherneck, Manfred Schwab
JournalCancer letters (Cancer Lett) Vol. 257 Issue 1 Pg. 65-72 (Nov 8 2007) ISSN: 0304-3835 [Print] Ireland
PMID17686574 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
Chemical References
  • Apoptosis Regulatory Proteins
  • BLID protein, human
  • BRCA2 Protein
  • BRCA2 protein, human
  • Cyclin-Dependent Kinase Inhibitor p21
  • E2F1 Transcription Factor
  • E2F1 protein, human
  • Nucleotides
  • Retinoblastoma Protein
  • AURKB protein, human
  • Aurora Kinase B
  • Aurora Kinases
  • Protein-Serine-Threonine Kinases
Topics
  • Alleles
  • Apoptosis Regulatory Proteins
  • Aurora Kinase B
  • Aurora Kinases
  • BRCA2 Protein (genetics, physiology)
  • Breast Neoplasms (genetics, metabolism, pathology)
  • Cell Cycle
  • Cell Nucleus (metabolism)
  • Cyclin-Dependent Kinase Inhibitor p21 (metabolism)
  • E2F1 Transcription Factor (metabolism)
  • Gene Expression Regulation, Neoplastic
  • Humans
  • In Situ Hybridization, Fluorescence
  • Nucleotides (chemistry)
  • Polyploidy
  • Protein-Serine-Threonine Kinases (metabolism)
  • Retinoblastoma Protein (metabolism)

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