Elevated level of cyclin D1 in mos-transformed cells.

Yang,Y; Pham,C D; Arlinghaus,R B; Khillan,J S; Singh,B

doi:10.3892/ijo.12.5.1199

May 1998 Volume 12 Issue 5

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May 1998 Volume 12 Issue 5

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Article

Elevated level of cyclin D1 in mos-transformed cells.

Authors:
- Y Yang
- C D Pham
- R B Arlinghaus
- J S Khillan
- B Singh
View Affiliations / Copyright

Affiliations: Department of Molecular Pathology, The University of Texas M.D. Anderson Cancer Center, Houston, TX 77030, USA.
Pages: 1199-1401
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Published online on: May 1, 1998

https://doi.org/10.3892/ijo.12.5.1199
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Abstract

Mos is a germ cell-specific serine/threonine protein kinase that plays an important role during meiotic divisions of oocytes. Upon expression in somatic cells, Mos causes cell cycle perturbations leading to neoplastic transformation. Mos activates the MAP kinase pathway in both oocytes and transformed somatic cells. To determine the mechanism of cell cycle perturbation in mos-transformed cells, we examined the status of some key regulators of G1 phase. We provide evidence that Mos causes an elevation in the level of cyclin D1 in NIH/3T3 cells. As expected from the increased cyclin D1 level, mos transformation of NIH/3T3 cells caused an increase in the protein kinase activities of cyclin D1-Cdk4 and cyclin E-Cdk2 and induced hyperphosphorylation of the retinoblastoma protein. Of importance, the level of cyclin D1 was also elevated in eye lens of the c-mos-transgenic mice compared to normal mice. Our results indicate that the mechanism of cellular transformation by Mos involves an elevation in the level of cyclin D1 in somatic cells.

Journals

International Journal of Molecular Medicine

International Journal of Oncology

Molecular Medicine Reports

Oncology Reports

Experimental and Therapeutic Medicine

Oncology Letters

Biomedical Reports

Molecular and Clinical Oncology

World Academy of Sciences Journal

International Journal of Functional Nutrition

International Journal of Epigenetics

Medicine International

Elevated level of cyclin D1 in mos-transformed cells.

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Abstract

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