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Journal of Biochemistry Advance Access published online on June 24, 2009
Journal of Biochemistry, doi:10.1093/jb/mvp092
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© The authors 2009. Published by Oxford University Press on behalf of the Japanese Biochemical Society. All rights reserved.

Overexpression of Plk3 causes morphological change and cell growth suppression in Ras pathway-activated cells

Masato Iida, Takanori Sasaki and Hideya Komatani*

Department of Oncology, Tsukuba Research Institute, Banyu Pharmaceutical Co., Ltd., Okubo 3, Tsukuba, Ibaraki 300-2611, Japan

*To whom correspondence should be addressed: Hideya Komatani. Department of Oncology, Tsukuba Research Institute, Banyu Pharmaceutical Co., Ltd. Okubo 3, Tsukuba, Ibaraki 300-2611, Japan Tel: 81-29-877-2000, Fax: 81-29-877-2027, E-mail: hideya_komatani{at}merck.com

Received May 28, 2009; Accepted June 11, 2009


  Abstract

To unravel the growth inhibition mechanism of Plk3, the effect of overexpression of Plk3 was examined in 293T cells. Cell rounding, changes in actin organization, and cellular detachment were induced by Plk3 transfection in a kinase activity-dependent manner. Although apoptosis was not observed, Plk3 overexpression suppressed cellular growth in a long-term colony-forming assay. Because both Plk3 and Ras affect f-actin organization, the effect of co-transfection of Plk3 and Ras was evaluated. Adhesion was synergistically lost by co-transfection of these two genes, compared with transfection of Plk3 alone. Furthermore, overexpression of Plk3 caused long-term growth suppression in Ras-transformed NIH3T3. Collectively, Plk3 activation might cause cytoskeleton re-organization and result in growth suppression more pronouncedly in Ras pathway-activated cells.

Key Words: Plk3, Overexpression, H-Ras, morphology, growth suppression


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