Cited by 34Cancer-related Molecular PathwaysMicrotubule and mitosis dynamicsCell death mechanisms and regulation

MdmX regulates transformation and chromosomal stability in p53-deficient cells

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Matijasevic, Zdenka, Krzywicka-Racka, Anna, Sluder, Greenfield, Jones, Stephen N.·2008·Cell Cycle

Abstract

The cellular homologues Mdm2 and MdmX play critical roles in regulating the activity of the p53 tumor suppressor in damaged and non-damaged cells and during development in mice. Recently, we have utilized genetically defined primary cells and mice to reveal that endogenous levels of MdmX can also suppress multipolar mitosis and transformation in hyperploid p53-deficient cells and tumorigenesis in p53-deficient mice. These MdmX functions are not shared by Mdm2, and are distinct from the well-established ability of MdmX to complex with and inhibit p53 activity. Here we discuss some of the ramifications of MdmX loss in p53-deficient cells and mice, and we explore further the fate of MdmX/p53-double null embryonic fibroblasts undergoing multi-polar cell division using time-lapse video microscopy. We also discuss the relationship between chromosomal loss, cell proliferation, and the tumorigenic potential of p53-deficient cells lacking MdmX.

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Authors
Matijasevic, Z., Krzywicka-Racka, A., Sluder, G., & Jones, S. N.
Affiliations
University of Massachusetts Chan Medical School (US)
Corresponding author
Jones, Stephen N.
Venue
Cell Cycle
Published
2008-10
Volume
7
Issue
19
Pages
2967-2973
ISSN
  • 1538-4101 (ISSN-L)
  • 1551-4005
OpenAlex
W2025966252
Cited by
34
References
76
Citations by year
2026: 1 · 2025: 1 · 2024: 1 · 2023: 1 · 2021: 1 · 2020: 2 · 2019: 1 · 2018: 1 · 2016: 6 · 2015: 2 · 2014: 5 · 2013: 3 · 2012: 4
FWCI
0.16
Type
journal article
Language
en
Open access
Locations
  • Cell Cycle (publishedVersion)
  • PubMed (publishedVersion)
  • PubMed Central (acceptedVersion)
  • The Journal of the American Medical Association (JAMA) Network (American Medical Association) (submittedVersion)
Funders
  • National Institutes of Health
  • National Cancer Institute (R01CA077735, R01CA77735)
  • National Institute of General Medical Sciences (R01GM30758, R01GM030758)
Topics
  • Health Sciences › Medicine › Oncology › Cancer-related Molecular Pathways
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Cell Biology › Microtubule and mitosis dynamics
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Cell death mechanisms and regulation
Keywords
MDMX, MDM2, p53, p53-deficient cells, chromosome stability, chromosome loss, multipolar mitosis, cell transformation, carcinogenesis, hyperploidy, embryonic fibroblasts, cell proliferation, tumor suppressor regulation
MeSH terms
Animals, Cell Division, Cell Transformation, Neoplastic, Humans, Mitosis, Tumor Suppressor Protein p53, Centrosome, Chromosomal Instability, Mice, Proto-Oncogene Proteins c-mdm2

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