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Genes to Cells (2005) 10, 655-663. doi:10.1111/j.1365-2443.2005.00866.x
© 2005 Blackwell Publishing or its licensors
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Activation of c-Jun amino-terminal kinase by GDNF induces G2/M cell cycle delay linked with actin reorganization

Toshifumi Fukuda1,{dagger}, Naoya Asai1, Atsushi Enomoto1 and Masahide Takahashi1,2,*

1 Department of Pathology, and 2 Division of Molecular Pathology, Center for Neurological Disease and Cancer, Nagoya University Graduate School of Medicine, 65 Tsurumai-cho, Showa-ku, Nagoya, 466-8550, Japan

It is well known that the cell cycle is controlled by several cyclin/cyclin-dependent kinase (Cdk) complexes whose expression and phosphorylation states vary with orderly periodicity. During the cell cycle, activity of the cyclin/Cdk complexes can be regulated directly or indirectly by a number of molecules, including protein kinases and phosphatases, p53, and Cdk inhibitors. Here, we show that the addition of glial cell line-derived neurotrophic factor (GDNF) induced G2/M cell cycle delay in human SK-N-MC neuroectodermal tumor cells that express RET tyrosine kinase, accompanying actin reorganization. Cell cycle delay at G2/M was characterized by accelerated and prolonged Cdc2 phosphorylation and stabilization of cyclin B1 and Wee1 kinase expression. Interestingly, we found that phosphorylation and/or expression of Cdc2, cyclinB1, and Wee1 was controlled by the Rac1/c-Jun NH2-terminal kinase (JNK) pathway. Immunohistochemical analysis suggested that the G2/M cell cycle delay may be necessary to prevent the mitotic progression of SK-N-MC cells with perturbed actin cytoskeletons.

Communicated by: Kozo Kaibuchi

{dagger}Present address: Department of Developmental Neurobiology, Institute of Development, Aging and Cancer, Tohoku University, 4-1, Seiryo, Aoba, Sendai 980-8575, Japan.

* Correspondence: E-mail: mtakaha{at}med.nagoya-u.ac.jp




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