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Elevated level of cyclin D1 in mos-transformed cells
Y Yang1, C D Pham, R B Arlinghaus
1Department of Molecular Pathology, The University of Texas M.D. Anderson Cancer Center, Houston, TX 77030, USA.
International Journal of Oncology
|June 6, 1998
Summary
Mos protein kinase, when expressed in somatic cells, disrupts the cell cycle and promotes neoplastic transformation. This transformation involves elevated cyclin D1 levels, impacting cell cycle regulators and leading to cellular changes observed in transgenic mice.
Area of Science:
- Oncology
- Cell Biology
- Molecular Biology
Background:
- Mos is a germ cell-specific kinase crucial for oocyte meiotic divisions.
- Aberrant Mos expression in somatic cells induces cell cycle perturbations and neoplastic transformation.
- Mos activates the mitogen-activated protein kinase (MAPK) pathway in both oocytes and transformed somatic cells.
Purpose of the Study:
- To elucidate the mechanism by which Mos induces cell cycle perturbations in transformed somatic cells.
- To investigate the role of key G1 phase regulators in Mos-mediated cellular transformation.
- To determine if Mos influences cyclin D1 levels in somatic cells and transgenic mouse models.
Main Methods:
- Examination of G1 phase regulators in NIH/3T3 cells expressing Mos.
- Analysis of cyclin D1 protein levels in Mos-transformed NIH/3T3 cells.
- Assessment of cyclin D1-Cdk4 and cyclin E-Cdk2 kinase activities.
- Evaluation of retinoblastoma protein phosphorylation status.
- Comparison of cyclin D1 levels in the eye lens of c-mos-transgenic mice and normal mice.
Main Results:
- Mos expression in NIH/3T3 cells leads to a significant elevation in cyclin D1 levels.
- Mos transformation increases the kinase activities of cyclin D1-Cdk4 and cyclin E-Cdk2 complexes.
- Hyperphosphorylation of the retinoblastoma protein is induced in Mos-transformed cells.
- Elevated cyclin D1 levels are also observed in the eye lens of c-mos-transgenic mice compared to controls.
Conclusions:
- Mos-mediated cellular transformation involves the upregulation of cyclin D1 in somatic cells.
- The elevation in cyclin D1 contributes to cell cycle dysregulation and neoplastic transformation.
- Mos's role in elevating cyclin D1 provides a mechanistic link between its expression and oncogenic potential.